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  • 1
    Electronic Resource
    Electronic Resource
    Lack of association between free testosterone and bone density separate from age in elderly males (1993)
    Springer
    Calcified tissue international 52 (1993), S. 67-69 
    Details
    ISSN: 1432-0827
    Keywords: Male ; Osteoporosis ; Free testosterone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary It is unclear what proportion of the variance in bone density in elderly males is accounted for by testosterone status. We studied 112 ambulatory, elderly volunteers (mean age 71.7 years) and determined free testosterone (FT), as well as bone density measurements by photon absorptiometry at multiple sites. Our studies of 35 of these subjects 4 years later includedmorning FT and dual energy X-ray absorptiometry. There were no significant correlations between FT and bone density at multiple scanning sites with the effects of age partialed out. We suspect that our inability to detect a significant effect of FT on bone density was related to the relative strength of other determinants of bone density, as well as to the fact that FT values are far more dynamic than bone density.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00675629
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of estrogen replacement on insulin-like growth factor I concentrations in serum and bone tissue and on interleukin 1 secretion from spleen macrophages in oophorectomized rats (1993)
    Springer
    Calcified tissue international 53 (1993), S. 111-116 
    Details
    ISSN: 1432-0827
    Keywords: Insulinlike growth factor I ; Interleukin 1 ; Oophorectomy ; Estrogen ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Oophorectomy (OOX) has been known to increase bone turnover, but its precise mechanism is not fully understood. In order to further investigate the mechanism, we determined insulinlike growth factor I (IGF-I) concentrations in serum and bone tissue and interleukin 1 (IL-1) release from spleen macrophages in oophorectomized rats because it has been demonstrated that IGF-I stimulates bone formation and IL-1 stimulates bone resorption. Female 8-week-old Wistar rats were divided into four groups: (1) control, (2) OOX, (3) OOX given estradiol, and (4) control given estradiol. Ten μg/kg of 17β-estradiol was given daily by subcutaneous injection. After 5 weeks of treatment, IGF-I concentrations in the extract from right femur and in serum were determined by specific radioimmunoassay. IL-1 activity released from lipopolysaccharide (LPS)-stimulated spleen macrophages was determined by bioassay. IGF-I contents in the femur and IGF-I concentrations in serum in oophorectomized rats were significantly higher than those in control rats. Treatment by estradiol inhibited the increase in IGF-I concentrations both in femur and in serum. IL-1 release from LPS-stimulated spleen macrophages in oophorectomized rats was increased, and treatment by estradiol also inhibited the stimulated IL-1 release. The ash weights and the calcium contents of left femur in oophorectomized rats were lower than those in control rats. These results suggest that both IGF-I and IL-1 may be involved in the mechanism of the regulation of bone turnover in oophorectomized rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01321888
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  • 3
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    Sea urchin egg receptor for sperm: sequence similarity of binding domain and hsp70 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: Fertilization depends on cell surface recognition proteins that interact and thereby mediate binding and subsequent fusion of the sperm and egg. Overlapping complementary DNA's encoding the egg plasma membrane receptor for sperm from the sea urchin Strongylocentrotus purpuratus were cloned and sequenced. Analysis of the deduced primary structure suggests that the receptor is a transmembrane protein with a short cytoplasmic domain. This domain showed no sequence similarity to known protein sequences. In contrast, the extracellular, sperm binding domain of the receptor did show sequence similarity to the heat shock protein 70 (hsp70) family of proteins. Recombinant protein representing this portion of the receptor bound to the sperm protein, binding, and also inhibited fertilization in a species-specific manner; beads coated with the protein became specifically bound to acrosome-reacted sperm. These data provide a basis for detailed investigations of molecular interactions that occur in gamete recognition and egg activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Foltz, K R -- Partin, J S -- Lennarz, W J -- HD18590/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1421-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of California, Santa Barbara 93106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8383878" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cloning, Molecular ; Female ; Fertilization ; Heat-Shock Proteins/*genetics ; Humans ; Male ; Molecular Sequence Data ; Ovum/physiology ; Receptors, Cell Surface/*genetics/metabolism ; Recombinant Proteins/metabolism ; Restriction Mapping ; Sea Urchins ; Sequence Homology, Amino Acid ; Sperm-Ovum Interactions ; Spermatozoa/cytology/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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  • 4
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    Role of intracellular calcium in NI-35-evoked collapse of neuronal growth cones (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: A myelin-associated protein from the central nervous system, the neurite growth inhibitor NI-35, inhibits regeneration of lesioned neuronal fiber tracts in vivo and growth of neurites in vitro. Growth cones of cultured rat dorsal root ganglion neurons arrested their growth and collapsed when exposed to liposomes containing NI-35. Before morphological changes, the concentration of free intracellular calcium ([Ca2+]i) showed a rapid and large increase in growth cones exposed to liposomes containing NI-35. Neither an increase in [Ca2+]i nor collapse of growth cones was detected in the presence of antibodies to NI-35. Dantrolene, an inhibitor of calcium release from caffeine-sensitive intracellular calcium stores, protected growth cones from collapse evoked by NI-35. Depletion of these caffeine-sensitive intracellular calcium stores prevented the increase in [Ca2+]i evoked by NI-35. The NI-35-evoked cascade of intracellular messengers that mediates collapse of growth cones includes the crucial step of calcium release from intracellular stores.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bandtlow, C E -- Schmidt, M F -- Hassinger, T D -- Schwab, M E -- Kater, S B -- NS24683/NS/NINDS NIH HHS/ -- NS28323/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):80-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brain Research Institute, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caffeine/pharmacology ; Calcium/*metabolism ; Cells, Cultured ; Drug Carriers ; Fura-2 ; Ganglia, Spinal/*physiology ; Growth Inhibitors/*pharmacology ; Kinetics ; Liposomes ; Nerve Fibers/drug effects/*physiology/ultrastructure ; Neurons/drug effects/*physiology/ultrastructure ; Rats
    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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    Somber news from the AIDS front (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1712-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8390093" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/therapeutic use ; *Acquired Immunodeficiency Syndrome/drug therapy/immunology/prevention & control ; Drug Therapy, Combination ; Female ; Humans ; Immunity, Cellular ; Male ; Sexually Transmitted Diseases/prevention & control ; Zalcitabine/therapeutic use ; Zidovudine/therapeutic use
    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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    Sex, violence, and sociobiology (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barash, D P -- New York, N.Y. -- Science. 1993 Oct 22;262(5133):491.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Child ; Child Abuse ; Female ; Humans ; Male ; *Sexual Behavior ; Sexual Behavior, Animal ; Sociology ; *Violence
    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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    Cue-invariant shape selectivity of macaque inferior temporal neurons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-14
    Description: The perception of shape is independent of the size and position of the shape and also of the visual cue that defines it. The same shape can be recognized whether defined by a difference in luminance, by motion, or by texture. Experiments showed that the shape selectivity of individual cells in the macaque inferior temporal cortex did not vary with the size and position of a shape and also did not vary with the visual cue used to define the shape. This cue invariance was true for static luminance and texture cues as well as for relative motion cues--that is, for cues that are processed in ventral and dorsal visual pathways. The properties of these inferior temporal cells meet the demands of cue-invariant shape coding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sary, G -- Vogels, R -- Orban, G A -- New York, N.Y. -- Science. 1993 May 14;260(5110):995-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratorium voor Neuro- en Psychofysiologie, Faculteit der Geneeskunde, Katholieke Universiteit Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493538" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Form Perception ; Light ; Macaca mulatta ; Male ; Movement ; Neurons/*physiology ; Temporal Lobe/*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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  • 8
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    Deletion of the paired alpha 5(IV) and alpha 6(IV) collagen genes in inherited smooth muscle tumors (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-27
    Description: The gene encoding alpha 6(IV) collagen, COL4A6, was identified on the human X chromosome in a head-to-head arrangement and within 452 base pairs of the alpha 5(IV) collagen gene, COL4A5. In earlier studies, intragenic deletions of COL4A5 were detected in a subset of patients with Alport syndrome (AS), a hereditary defect of basement membranes. In some families, AS cosegregates with diffuse leiomyomatosis (DL), a benign smooth muscle tumor diathesis. Here it is shown that patients with AS-DL harbor deletions that disrupt both COL4A5 and COL4A6. Thus, type IV collagen may regulate smooth muscle differentiation and morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, J -- Mochizuki, T -- Smeets, H -- Antignac, C -- Laurila, P -- de Paepe, A -- Tryggvason, K -- Reeders, S T -- New York, N.Y. -- Science. 1993 Aug 27;261(5125):1167-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06536-0812.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8356449" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Differentiation ; Collagen/chemistry/*genetics ; Exons ; Female ; Fetus/metabolism ; *Gene Deletion ; Genetic Linkage ; Humans ; Leiomyoma/*genetics ; Male ; Molecular Sequence Data ; Morphogenesis ; Muscle, Smooth/cytology ; Mutation ; Nephritis, Hereditary/*genetics ; RNA, Messenger/genetics/metabolism
    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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    Expression cloning and signaling properties of the rat glucagon receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-12
    Description: Glucagon and the glucagon receptor are a primary source of control over blood glucose concentrations and are especially important to studies of diabetes in which the loss of control over blood glucose concentrations clinically defines the disease. A complementary DNA clone for the glucagon receptor was isolated by an expression cloning strategy, and the receptor protein was expressed in several kidney cell lines. The cloned receptor bound glucagon and caused an increase in the intracellular concentration of adenosine 3', 5'-monophosphate (cAMP). The cloned glucagon receptor also transduced a signal that led to an increased concentration of intracellular calcium. The glucagon receptor is similar to the calcitonin and parathyroid hormone receptors. It can transduce signals leading to the accumulation of two different second messengers, cAMP and calcium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jelinek, L J -- Lok, S -- Rosenberg, G B -- Smith, R A -- Grant, F J -- Biggs, S -- Bensch, P A -- Kuijper, J L -- Sheppard, P O -- Sprecher, C A -- New York, N.Y. -- Science. 1993 Mar 12;259(5101):1614-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ZymoGenetics Inc., Seattle, WA 98105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8384375" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/pharmacology ; Cell Line ; Cloning, Molecular ; Cricetinae ; Cyclic AMP/metabolism ; Glucagon/metabolism/*pharmacology ; Kidney ; Kinetics ; Liver/*metabolism ; Molecular Sequence Data ; Rats ; Receptors, Gastrointestinal Hormone/genetics/metabolism/*physiology ; Receptors, Glucagon ; *Signal Transduction ; Transfection
    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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    Inhibition by cAMP of Ras-dependent activation of Raf (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-12
    Description: Activation of the Raf and extracellular signal-regulated kinases (ERKs) (or mitogen-activated protein kinases) are key events in mitogenic signalling, but little is known about interactions with other signaling pathways. Agents that raise levels of intracellular cyclic adenosine 3',5'-monophosphate (cAMP) blocked DNA synthesis and signal transduction in Rat1 cells exposed to epidermal growth factor (EGF) or lysophosphatidic acid. In the case of EGF, receptor tyrosine kinase activity and association with the signaling molecules Grb2 and Shc were unaffected by cAMP. Likewise, EGF-dependent accumulation of the guanosine 5'-triphosphate-bound form of Ras was unaffected. In contrast, activation of Raf-1 and ERK kinases was inhibited. Thus, cAMP appears to inhibit signal transmission from Ras by preventing Ras-dependent activation of Raf-1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, S J -- McCormick, F -- UO1 CA51992-03/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Nov 12;262(5136):1069-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Onyx Pharmaceuticals, Richmond, CA 94806.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694367" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; Animals ; Bucladesine/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Cholera Toxin/pharmacology ; Cyclic AMP/*pharmacology ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Enzyme Activation ; Epidermal Growth Factor/pharmacology ; Interphase ; Lysophospholipids/pharmacology ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Proto-Oncogene Proteins p21(ras)/*metabolism ; Rats ; Receptor, Epidermal Growth Factor/metabolism ; *Signal Transduction
    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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  • 11
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    Microsatellite instability in cancer of the proximal colon (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-07
    Description: Colorectal tumor DNA was examined for somatic instability at (CA)n repeats on human chromosomes 5q, 15q, 17p, and 18q. Differences between tumor and normal DNA were detected in 25 of the 90 (28 percent) tumors examined. This instability appeared as either a substantial change in repeat length (often heterogeneous in nature) or a minor change (typically two base pairs). Microsatellite instability was significantly correlated with the tumor's location in the proximal colon (P = 0.003), with increased patient survival (P = 0.02), and, inversely, with loss of heterozygosity for chromosomes 5q, 17p, and 18q. These data suggest that some colorectal cancers may arise through a mechanism that does not necessarily involve loss of heterozygosity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thibodeau, S N -- Bren, G -- Schaid, D -- CA-15083-18E8.1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 7;260(5109):816-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics Laboratory, Mayo Clinic, Rochester, MN 55905.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484122" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Chromosomes, Human, Pair 15 ; Chromosomes, Human, Pair 17 ; Chromosomes, Human, Pair 18 ; Chromosomes, Human, Pair 5 ; Colonic Neoplasms/*genetics ; Colorectal Neoplasms/*genetics ; DNA, Neoplasm/*genetics ; DNA, Satellite/*genetics ; Female ; Heterozygote ; Humans ; Male ; Middle Aged ; *Mutation ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid
    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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  • 12
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    A genetic linkage map of the mouse: current applications and future prospects (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-01
    Description: Technological advances have made possible the development of high-resolution genetic linkage maps for the mouse. These maps in turn offer exciting prospects for understanding mammalian genome evolution through comparative mapping, for developing mouse models of human disease, and for identifying the function of all genes in the organism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Copeland, N G -- Jenkins, N A -- Gilbert, D J -- Eppig, J T -- Maltais, L J -- Miller, J C -- Dietrich, W F -- Weaver, A -- Lincoln, S E -- Steen, R G -- HG00198/HG/NHGRI NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):57-66.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211130" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Chromosome Mapping ; Cloning, Molecular ; Crosses, Genetic ; Female ; Genetic Markers ; *Genome ; Human Genome Project ; Humans ; Male ; Mice/*genetics ; Multigene Family ; Muridae/*genetics ; Mutation ; Neoplasms/genetics
    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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  • 13
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    Blood-brain barrier penetration and in vivo activity of an NGF conjugate (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-15
    Description: Nerve growth factor (NGF) is essential for the survival of both peripheral ganglion cells and central cholinergic neurons of the basal forebrain. The accelerated loss of central cholinergic neurons during Alzheimer's disease may be a determinant of dementia in these patients and may therefore suggest a therapeutic role for NGF. However, NGF does not significantly penetrate the blood-brain barrier, which makes its clinical utility dependent on invasive neurosurgical procedures. When conjugated to an antibody to the transferrin receptor, however, NGF crossed the blood-brain barrier after peripheral injection. This conjugated NGF increased the survival of both cholinergic and noncholinergic neurons of the medial septal nucleus that had been transplanted into the anterior chamber of the rat eye. This approach may prove useful for the treatment of Alzheimer's disease and other neurological disorders that are amenable to treatment by proteins that do not readily cross the blood-brain barrier.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friden, P M -- Walus, L R -- Watson, P -- Doctrow, S R -- Kozarich, J W -- Backman, C -- Bergman, H -- Hoffer, B -- Bloom, F -- Granholm, A C -- NS29601-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):373-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Alkermes, Inc., Cambridge, MA 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8420006" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Chamber/metabolism ; Antibodies/*metabolism ; *Blood-Brain Barrier ; Brain/blood supply/metabolism ; Capillaries ; Cell Line ; Cross-Linking Reagents ; Dose-Response Relationship, Drug ; Drug Carriers ; Immunohistochemistry ; Nerve Growth Factors/administration & dosage/*pharmacokinetics/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Transferrin/*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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  • 14
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    A detailed genetic map for the X chromosome of the malaria vector, Anopheles gambiae (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-30
    Description: Anopheles gambiae, the primary vector of human malaria in Africa, is responsible for approximately a million deaths per year, mostly of children. Despite its significance in disease transmission, this mosquito has not been studied extensively by genetic or molecular techniques. To facilitate studies on this vector, a genetic map has been developed that covers the X chromosome at an average resolution of 2 centimorgans. This map has been integrated with the chromosome banding pattern and used to localize a recessive, sex-linked mutation (white eye) to within 1 centimorgan of flanking markers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, L -- Collins, F H -- Kumar, V -- Kafatos, F C -- New York, N.Y. -- Science. 1993 Jul 30;261(5121):605-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Developmental Biology, Harvard University, Cambridge, MA 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342025" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Anopheles/*genetics ; Base Sequence ; Chromosome Banding ; *Chromosome Mapping ; Crosses, Genetic ; DNA, Satellite/genetics ; Female ; *Genes, Insect ; Genes, Recessive ; Genetic Markers ; Insect Vectors/*genetics ; Malaria/transmission ; Male ; Molecular Sequence Data ; Mutation ; Recombination, Genetic ; *X Chromosome
    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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  • 15
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    Altered fluid transport across airway epithelium in cystic fibrosis (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-15
    Description: In cystic fibrosis (CF), absence or dysfunction of a phosphorylation-regulated chloride channel [CF transmembrane conductance regulator (CFTR)] leads to the loss or reduction of chloride secretion into the airways. Active sodium absorption is also increased in CF, and both of these ion transport changes could alter fluid transport across the airways. Under baseline conditions, cultured human airway epithelia from normal individuals absorbed fluid, and this absorption was increased in epithelia from patients with CF. In normal and CF epithelial cultures fluid absorption was inhibited by amiloride. Adenosine 3',5'-monophosphate stimulated fluid secretion in normal epithelial cultures but not in cultures from individuals with CF. In contrast, fluid secretion induced by nucleotide triphosphates (uridine triphosphate or adenosine triphosphate) was unaltered in cultures of epithelia from patients with CF, suggesting an approach to the treatment of CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, C -- Finkbeiner, W E -- Widdicombe, J H -- McCray, P B Jr -- Miller, S S -- HL 42368/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 15;262(5132):424-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211164" target="_blank"〉PubMed〈/a〉
    Keywords: Absorption ; Adenosine Triphosphate/pharmacology ; Adolescent ; Adult ; Amiloride/pharmacology ; Body Fluids/*metabolism ; Cells, Cultured ; Cyclic AMP/pharmacology ; Cystic Fibrosis/*metabolism ; Epithelial Cells ; Epithelium/metabolism ; Female ; Humans ; Male ; Middle Aged ; Nasal Mucosa/cytology/*metabolism ; Sodium/metabolism ; Sodium Channels/metabolism ; Trachea/cytology/*metabolism ; Uridine Triphosphate/pharmacology
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    Selective and ATP-dependent translocation of peptides by the MHC-encoded transporter (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-06
    Description: Major histocompatibility complex (MHC) class I molecules present peptides derived from nuclear and cytosolic proteins to CD8+ T cells. These peptides are translocated into the lumen of the endoplasmic reticulum (ER) to associate with class I molecules. Two MHC-encoded putative transporter proteins, TAP1 and TAP2, are required for efficient assembly of class I molecules and presentation of endogenous peptides. Expression of TAP1 and TAP2 in a mutant cell line resulted in the delivery of an 11-amino acid oligomer model peptide to the ER. Peptide translocation depended on the sequence of the peptide, was adenosine triphosphate (ATP)-dependent, required ATP hydrolysis, and was inhibited in a concentration-dependent manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neefjes, J J -- Momburg, F -- Hammerling, G J -- New York, N.Y. -- Science. 1993 Aug 6;261(5122):769-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Netherlands Cancer Institute, Amsterdam.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342042" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Adenosine Triphosphate/*metabolism ; Amino Acid Sequence ; Animals ; Biological Transport ; Carrier Proteins/*metabolism ; Cell Line ; Cell Membrane Permeability ; Endoplasmic Reticulum/metabolism ; Glycosylation ; Histocompatibility Antigens Class II/*metabolism ; Molecular Sequence Data ; Oligopeptides/*metabolism ; Rats ; T-Lymphocytes, Cytotoxic/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cloning the differences between two complex genomes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-12
    Description: The analysis of the differences between two complex genomes holds promise for the discovery of infectious agents and probes useful for genetic studies. A system was developed in which subtractive and kinetic enrichment was used to purify restriction endonuclease fragments present in one population of DNA fragments but not in another. Application of this method to DNA populations of reduced complexity ("representations") resulted in the isolation of probes to viral genomes present as single copies in human DNA, and probes that detect polymorphisms between two individuals. In principle, this system, called representational difference analysis (RDA), may also be used for isolating probes linked to sites of genomic rearrangements, whether occurring spontaneously and resulting in genetic disorders or cancer, or programmed during differentiation and development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lisitsyn, N -- Wigler, M -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):946-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, NY 11724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8438152" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Bacteriophage lambda/genetics ; Base Sequence ; *Cloning, Molecular ; DNA/*chemistry ; DNA Probes ; DNA, Viral ; Female ; Gene Deletion ; Genetic Diseases, Inborn/genetics ; Humans ; Male ; Molecular Sequence Data ; Neoplasms/genetics ; Nucleic Acid Hybridization/methods ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Sequence Homology, Nucleic Acid
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Higher level organization of individual gene transcription and RNA splicing (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-26
    Description: Visualization of fibronectin and neurotensin messenger RNAs within mammalian interphase nuclei was achieved by fluorescence hybridization with genomic, complementary DNA, and intron-specific probes. Unspliced transcripts accumulated in one or two sites per nucleus. Fibronectin RNA frequently accumulated in elongated tracks that overlapped and extended well beyond the site of transcription. Splicing appears to occur directly within this RNA track, as evidenced by an unambiguous spatial separation of intron-containing and spliced transcripts. Excised introns for neurotensin RNA appear free to diffuse. The transcription and processing site of the fibronectin gene localized to the nuclear interior and was associated with larger transcript domains in over 88 percent of the cells. These results support a view of nuclear function closely integrated with structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xing, Y -- Johnson, C V -- Dobner, P R -- Lawrence, J B -- R01 HG00251/HG/NHGRI NIH HHS/ -- R01 HL33307/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1326-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, University of Massachusetts Medical Center, Worcester 01655.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8446901" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/metabolism/*ultrastructure ; Fibronectins/genetics ; Gene Expression ; In Vitro Techniques ; Introns ; Microscopy, Fluorescence ; Neurotensin/genetics ; PC12 Cells ; Poly A/metabolism ; *RNA Processing, Post-Transcriptional ; RNA Splicing ; RNA, Messenger/*metabolism ; Rats ; Spliceosomes/metabolism ; *Transcription, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A mechanism for virilization of female spotted hyenas in utero (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: Female spotted hyenas exhibit male-like genitalia and dominance over males. Hyena ovarian tissues incubated in vitro produced large quantities of the steroid hormone precursor androstenedione. The activity of aromatase, which converts androstenedione to estrogen, was one-twentieth as great in hyena versus human placental homogenates. In comparison, the activity of 17 beta-hydroxysteroid dehydrogenase, which converts androstenedione to testosterone, was equal in the two homogenates. The limited aromatase activity may allow the hyena placenta to convert high circulating concentrations of androstenedione to testosterone, which results in virilization of the fetal external genitalia and possibly destruction of fetal ovarian follicles. Androstenedione production by residual ovarian stromal cells during reproductive life accounts for the epigenetic transmission of virilization in female spotted hyenas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yalcinkaya, T M -- Siiteri, P K -- Vigne, J L -- Licht, P -- Pavgi, S -- Frank, L G -- Glickman, S E -- CA-39825/CA/NCI NIH HHS/ -- MH-39917/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1929-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics, Gynecology, University of California School of Medicine, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8391165" target="_blank"〉PubMed〈/a〉
    Keywords: 17-Hydroxysteroid Dehydrogenases/metabolism ; Animals ; Aromatase/*metabolism ; Carnivora/embryology/*metabolism ; Corpus Luteum/metabolism ; Estradiol/biosynthesis ; Female ; Humans ; In Vitro Techniques ; Luteinizing Hormone/pharmacology ; Male ; Ovary/*metabolism ; Placenta/enzymology/*metabolism ; Pregnancy ; Progesterone/biosynthesis ; *Sex Differentiation ; Testosterone/*biosynthesis
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  • 20
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    An adenovirus vector for gene transfer into neurons and glia in the brain (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-02-12
    Description: The efficient introduction of genetic material into quiescent nerve cells is important in the study of brain function and for gene therapy of neurological disorders. A replication-deficient adenoviral vector that contained a reporter gene encoding beta-galactosidase infected rat nerve cells in vitro and in vivo. beta-Galactosidase was expressed in almost all sympathetic neurons and astrocytes in culture. After stereotactic inoculations into the rat hippocampus and the substantia nigra, beta-galactosidase activity was detected for 2 months. Infected cells were identified as microglial cells, astrocytes, or neurons with anatomical, morphological, and immunohistochemical criteria. No obvious cytopathic effect was observed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Le Gal La Salle, G -- Robert, J J -- Berrard, S -- Ridoux, V -- Stratford-Perricaudet, L D -- Perricaudet, M -- Mallet, J -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):988-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Alfred Fessard, Unite Propre de Recherche 2212, Centre National de la Recherche Scientifique (CNRS), Gif sur Yvette, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8382374" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/*genetics ; Animals ; Astrocytes/metabolism/microbiology ; Avian Sarcoma Viruses/genetics ; Brain/*cytology ; DNA/genetics ; Gene Expression ; *Genetic Vectors ; Hippocampus/cytology/metabolism ; Neuroglia/*metabolism/microbiology ; Neurons/*metabolism/microbiology ; Promoter Regions, Genetic/genetics ; Rats ; Substantia Nigra/cytology/metabolism ; *Transfection ; beta-Galactosidase/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Australian pest control by virus causes concern (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, V -- New York, N.Y. -- Science. 1993 Aug 6;261(5122):683-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342036" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Australia ; Contraception, Immunologic/*veterinary ; Ecology ; Female ; *Foxes/microbiology ; *Genetic Engineering ; Male ; Myxoma virus/genetics ; Pest Control, Biological/*methods ; *Rabbits/microbiology ; Viruses/*genetics
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  • 22
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    Reversal of left-right asymmetry: a situs inversus mutation (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-04-30
    Description: A recessive mutation was identified in a family of transgenic mice that resulted in a reversal of left-right polarity (situs inversus) in 100 percent of the homozygous transgenic mice tested. Sequences that flanked the transgenic integration site were cloned and mapped to mouse chromosome 4, between the Tsha and Hxb loci. During early embryonic development, the direction of postimplantation turning, one of the earliest manifestations of left-right asymmetry, was reversed in homozygous transgenic embryos. This insertional mutation identifies a gene that controls embryonic turning and visceral left-right polarity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokoyama, T -- Copeland, N G -- Jenkins, N A -- Montgomery, C A -- Elder, F F -- Overbeek, P A -- HD25340/HD/NICHD NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480178" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Chromosome Mapping ; Cloning, Molecular ; Embryonic and Fetal Development/*genetics ; Female ; *Genes, Recessive ; Homozygote ; Male ; Mice ; Mice, Transgenic ; Mutagenesis, Insertional ; Situs Inversus/*genetics
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    Evidence found for a possible 'aggression gene' (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-06-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, V -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1722-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8511575" target="_blank"〉PubMed〈/a〉
    Keywords: *Aggression ; Female ; *Genes, Recessive ; Genetic Diseases, Inborn ; Humans ; Male ; Monoamine Oxidase/deficiency/*genetics ; Mutation ; Pedigree ; *X Chromosome
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  • 24
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    Retinoic acid stimulates regeneration of mammalian auditory hair cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-30
    Description: Sensorineural hearing loss resulting from the loss of auditory hair cells is thought to be irreversible in mammals. This study provides evidence that retinoic acid can stimulate the regeneration in vitro of mammalian auditory hair cells in ototoxic-poisoned organ of Corti explants in the rat. In contrast, treatment with retinoic acid does not stimulate the formation of extra hair cells in control cultures of Corti's organ. Retinoic acid-stimulated hair cell regeneration can be blocked by cytosine arabinoside, which suggests that a period of mitosis is required for the regeneration of auditory hair cells in this system. These results provide hope for a recovery of hearing function in mammals after auditory hair cell damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lefebvre, P P -- Malgrange, B -- Staecker, H -- Moonen, G -- Van de Water, T R -- DC00088/DC/NIDCD NIH HHS/ -- NS07098/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):692-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Physiology and Pathophysiology, University of Liege, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480180" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytarabine/pharmacology ; Hair Cells, Auditory/*drug effects/physiology/ultrastructure ; Microscopy, Electron ; Neomycin/toxicity ; Organ Culture Techniques ; Organ of Corti/*drug effects/physiology/ultrastructure ; Rats ; Regeneration/*drug effects ; Tretinoin/*pharmacology
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    MHC-restricted depletion of human myelin basic protein-reactive T cells by T cell vaccination (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Activated autoreactive T cells are potentially pathogenic and regulated by clonotypic networks. Experimental autoimmune diseases can be treated by inoculation with autoreactive T cells (T cell vaccination). In the present study, patients with multiple sclerosis were inoculated with irradiated myelin basic protein (MBP)-reactive T cells. T cell responses to the inoculates were induced to deplete circulating MBP-reactive T cells in the recipients. Regulatory T cell lines isolated from the recipients inhibited T cells used for vaccination. The cytotoxicity of the CD8+ T cell lines was restricted by major histocompatibility antigens. Thus, clonotypic interactions regulating autoreactive T cells in humans can be induced by T cell vaccination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Medaer, R -- Stinissen, P -- Hafler, D -- Raus, J -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1451-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Multiple Sclerosis Research Unit, Dr. L. Willems Instituut, Diepenbeek, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7690157" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Cell Line ; Epitopes/immunology ; Female ; Humans ; *Immunotherapy, Adoptive ; Lymphocyte Activation ; Male ; Middle Aged ; Multiple Sclerosis/immunology/*therapy ; Myelin Basic Protein/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/*immunology ; Vaccination
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  • 26
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    Effects of cAMP simulate a late stage of LTP in hippocampal CA1 neurons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-11
    Description: Hippocampal long-term potentiation (LTP) is thought to serve as an elementary mechanism for the establishment of certain forms of explicit memory in the mammalian brain. As is the case with behavioral memory, LTP in the CA1 region has stages: a short-term early potentiation lasting 1 to 3 hours, which is independent of protein synthesis, precedes a later, longer lasting stage (L-LTP), which requires protein synthesis. Inhibitors of cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) blocked L-LTP, and analogs of cAMP induced a potentiation that blocked naturally induced L-LTP. The action of the cAMP analog was blocked by inhibitors of protein synthesis. Thus, activation of PKA may be a component of the mechanism that generates L-LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frey, U -- Huang, Y Y -- Kandel, E R -- GM32099/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 11;260(5114):1661-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, Howard Hughes Medical Institute, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8389057" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects/physiology ; Animals ; Cyclic AMP/*physiology ; Hippocampus/cytology/drug effects/*physiology ; In Vitro Techniques ; Male ; Memory/physiology ; Neurons/drug effects/*physiology ; Protein Kinases/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/physiology ; Second Messenger Systems/physiology ; Time Factors
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  • 27
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    GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: A potent neurotrophic factor that enhances survival of midbrain dopaminergic neurons was purified and cloned. Glial cell line-derived neurotrophic factor (GDNF) is a glycosylated, disulfide-bonded homodimer that is a distantly related member of the transforming growth factor-beta superfamily. In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake. These effects were relatively specific; GDNF did not increase total neuron or astrocyte numbers nor did it increase transmitter uptake by gamma-aminobutyric-containing and serotonergic neurons. GDNF may have utility in the treatment of Parkinson's disease, which is marked by progressive degeneration of midbrain dopaminergic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, L F -- Doherty, D H -- Lile, J D -- Bektesh, S -- Collins, F -- New York, N.Y. -- Science. 1993 May 21;260(5111):1130-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Synergen, Inc., Boulder, CO 80301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Astrocytes/cytology/drug effects ; Base Sequence ; Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; Cloning, Molecular ; Dopamine/*biosynthesis ; Glial Cell Line-Derived Neurotrophic Factor ; Humans ; Mesencephalon/cytology/*drug effects/metabolism ; Molecular Sequence Data ; Molecular Weight ; *Nerve Growth Factors ; Nerve Tissue Proteins/chemistry/genetics/isolation & purification/*pharmacology ; Neuroglia/*metabolism ; Neurons/cytology/*drug effects/metabolism ; Parkinson Disease/drug therapy ; Rats
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  • 28
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    Genetic models for studying cancer susceptibility (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friend, S H -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):774-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Genetics, Massachusetts General Hospital Cancer Center, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430329" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crosses, Genetic ; Cyprinodontiformes/*genetics ; Female ; Fish Diseases/*genetics ; Genes, Tumor Suppressor ; *Genetic Predisposition to Disease ; Male ; Melanoma/genetics/*veterinary ; Models, Genetic ; Neoplasms/*genetics ; Proto-Oncogenes
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Genotypic and phenotypic characterization of HIV-1 patients with primary infection (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-27
    Description: Better characterization of human immunodeficiency virus-type 1 (HIV-1) in patients with primary infection has important implications for the development of an acquired immunodeficiency syndrome (AIDS) vaccine because vaccine strategies should target viral isolates with the properties of transmitted viruses. In five HIV-1 seroconverters, the viral phenotype was found to be uniformly macrophage-tropic and non-syncytium-inducing. Furthermore, the viruses were genotypically homogeneous within each patient, but a common signature sequence was not discernible among transmitted viruses. In the two cases where the sexual partners were also studied, the sequences of the transmitted viruses matched best with minor variants in the blood of the transmitters. There was also a stronger pressure to conserve sequences in gp120 than in gp41, nef, and p17, suggesting that a selective mechanism is involved in transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, T -- Mo, H -- Wang, N -- Nam, D S -- Cao, Y -- Koup, R A -- Ho, D D -- AI24030/AI/NIAID NIH HHS/ -- AI25541/AI/NIAID NIH HHS/ -- AI27742/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Aug 27;261(5125):1179-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aaron Diamond AIDS Research Center, New York University School of Medicine, NY 10016.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8356453" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Female ; Gene Products, gag/chemistry/genetics ; Genes, Viral ; Genotype ; Giant Cells/physiology ; HIV Antigens/chemistry/genetics ; HIV Envelope Protein gp120/chemistry/*genetics ; HIV Envelope Protein gp41/chemistry/genetics ; HIV Infections/*microbiology/transmission ; HIV Seropositivity/microbiology ; HIV-1/chemistry/*genetics/*physiology ; Humans ; Macrophages ; Male ; Molecular Sequence Data ; Phenotype ; Sequence Alignment ; Sexual Partners ; *Viral Proteins ; Virus Replication ; gag Gene Products, Human Immunodeficiency Virus
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    Clues to the pathogenesis of familial colorectal cancer (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-07
    Description: A predisposition to colorectal cancer is shown to be linked to markers on chromosome 2 in some families. Molecular features of "familial" cancers were compared with those of sporadic colon cancers. Neither the familial nor sporadic cancers showed loss of heterozygosity for chromosome 2 markers, and the incidence of mutations in KRAS, P53, and APC was similar in the two groups of tumors. Most of the familial cancers, however, had widespread alterations in short repeated DNA sequences, suggesting that numerous replication errors had occurred during tumor development. Thirteen percent of sporadic cancers had identical abnormalities and these cancers shared biologic properties with the familial cases. These data suggest a mechanism for familial tumorigenesis different from that mediated by classic tumor suppressor genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aaltonen, L A -- Peltomaki, P -- Leach, F S -- Sistonen, P -- Pylkkanen, L -- Mecklin, J P -- Jarvinen, H -- Powell, S M -- Jen, J -- Hamilton, S R -- CA 35494/CA/NCI NIH HHS/ -- CA 47527/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 7;260(5109):812-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Genetics, University of Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484121" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; *Chromosomes, Human, Pair 2 ; Colonic Neoplasms/*genetics ; Colorectal Neoplasms/*genetics ; DNA, Satellite/genetics ; Female ; Genetic Markers ; Humans ; Lod Score ; Male ; Mutation ; Pedigree ; Polymorphism, Genetic ; Rectal Neoplasms/genetics ; Repetitive Sequences, Nucleic Acid
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    Molecular cloning of an apolipoprotein B messenger RNA editing protein (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-18
    Description: Mammalian apolipoprotein B (apo B) exists in two forms, each the product of a single gene. The shorter form, apo B48, arises by posttranscriptional RNA editing whereby cytidine deamination produces a UAA termination codon. A full-length complementary DNA clone encoding an apo B messenger RNA editing protein (REPR) was isolated from rat small intestine. The 229-residue protein contains consensus phosphorylation sites and leucine zipper domains. HepG2 cell extracts acquire editing activity when mixed with REPR from oocyte extracts. REPR is essential for apo B messenger RNA editing, and the isolation and characterization of REPR may lead to the identification of other eukaryotic RNA editing proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Teng, B -- Burant, C F -- Davidson, N O -- DK-42086/DK/NIDDK NIH HHS/ -- HL-38180/HL/NHLBI NIH HHS/ -- KO-4 HL-02166/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1816-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8511591" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apolipoproteins B/*genetics ; Base Sequence ; Cell Line ; *Cloning, Molecular ; Cytidine Deaminase/chemistry/*genetics ; Humans ; Intestine, Small/chemistry ; Leucine Zippers ; Molecular Sequence Data ; Molecular Weight ; Open Reading Frames ; Phosphorylation ; *RNA Editing ; Rats ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The pluses of subtraction (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, R M -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):942-3.〈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/8094900" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/*chemistry ; DNA Probes ; Female ; Gene Deletion ; Humans ; Male ; Nucleic Acid Hybridization/*methods ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length
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    Progression to diabetes in nonobese diabetic (NOD) mice with transgenic T cell receptors (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-19
    Description: The T cell receptor (TCR) requirements in the pathogenesis of insulin-dependent diabetes were examined with transgenic NOD mice bearing nondisease-related TCR alpha and beta chains. In both TCR beta and TCR alpha beta transgenic NOD mice the beta chain transgene was expressed by 〉 98% of peripheral T cells. The alpha chain transgene was also highly expressed. Insulitis developed in both sets of transgenic animals with most of the lymphocytes in the lesion expressing the transgenic beta chain and with depletion of the endogenous TCR V beta genes. Nonetheless, NOD animals transgenic for TCR beta and TCR alpha beta developed diabetes similar to controls. Thus, skewing the TCR repertoire did not diminish autoimmune susceptibility in NOD mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipes, M A -- Rosenzweig, A -- Tan, K N -- Tanigawa, G -- Ladd, D -- Seidman, J G -- Eisenbarth, G S -- New York, N.Y. -- Science. 1993 Feb 19;259(5098):1165-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joslin Diabetes Center, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8267690" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Animals ; Base Sequence ; Crosses, Genetic ; Diabetes Mellitus, Type 2/genetics/immunology/*physiopathology ; Female ; Gene Rearrangement, T-Lymphocyte ; Islets of Langerhans/immunology/pathology ; Male ; Mice ; Mice, Inbred NOD/*physiology ; Mice, Transgenic ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Pancreatic Diseases/genetics/immunology/pathology ; Polymerase Chain Reaction/methods ; Receptors, Antigen, T-Cell, alpha-beta/genetics/*physiology ; T-Lymphocytes/*immunology/pathology
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    Dormancy of inhibitory interneurons in a model of temporal lobe epilepsy (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: In humans temporal lobe epilepsy (TLE) is characterized by recurrent seizures, neuronal hyperexcitability, and selective loss of certain neuronal populations in the hippocampus. Animal models of the condition indicate that a diminution of inhibition mediated by gamma-aminobutyric acid (GABA) accounts for the altered function, and it has been hypothesized that the diminution arises because GABAergic basket interneurons are "dormant" as a result of their being disconnected from excitatory inputs. In hippocampal slices, inhibitory postsynaptic potentials (IPSPs) were elicited in CA1 pyramidal cells by activation of basket cells; responses from an animal model of TLE were compared to those from control tissue. IPSPs evoked indirectly by activation of terminals that then excited basket cells were reduced in the epileptic tissue, whereas IPSPs evoked by direct activation of basket cells, when excitatory neurotransmission was blocked, were not different from controls. These results provide support for the "dormant basket cell" hypothesis and have implications for the pathophysiology and treatment of human TLE.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bekenstein, J W -- Lothman, E W -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):97-100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of Virginia Health Sciences Center, Charlottesville 22908.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8093417" target="_blank"〉PubMed〈/a〉
    Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione ; Action Potentials ; Animals ; Baclofen/analogs & derivatives/pharmacology ; Electric Stimulation ; Epilepsy, Temporal Lobe/*physiopathology ; Evoked Potentials ; Hippocampus/*physiology/*physiopathology ; In Vitro Techniques ; Interneurons/drug effects/*physiology ; Male ; Membrane Potentials ; Picrotoxin/pharmacology ; Pyramidal Tracts/drug effects/*physiology ; Quinoxalines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-A/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Status Epilepticus/*physiopathology
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    Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-13
    Description: The apolipoprotein E type 4 allele (APOE-epsilon 4) is genetically associated with the common late onset familial and sporadic forms of Alzheimer's disease (AD). Risk for AD increased from 20% to 90% and mean age at onset decreased from 84 to 68 years with increasing number of APOE-epsilon 4 alleles in 42 families with late onset AD. Thus APOE-epsilon 4 gene dose is a major risk factor for late onset AD and, in these families, homozygosity for APOE-epsilon 4 was virtually sufficient to cause AD by age 80.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corder, E H -- Saunders, A M -- Strittmatter, W J -- Schmechel, D E -- Gaskell, P C -- Small, G W -- Roses, A D -- Haines, J L -- Pericak-Vance, M A -- New York, N.Y. -- Science. 1993 Aug 13;261(5123):921-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Joseph and Kathleen Bryan Alzheimer's Disease Research Center, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8346443" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Aging ; *Alleles ; Alzheimer Disease/*genetics/metabolism/mortality ; Amyloid beta-Peptides/metabolism ; Apolipoprotein E4 ; Apolipoproteins E/*genetics/physiology ; Female ; *Gene Frequency ; Genotype ; Homozygote ; Humans ; Linkage Disequilibrium ; Male ; Risk Factors ; Survival Rate
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    Enhancement by histamine of NMDA-mediated synaptic transmission in the hippocampus (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-02
    Description: Histamine is a neuromodulator in the brain, and the hippocampus is one of the regions of the brain that is innervated by histaminergic neurons. When applied to cultured hippocampal neurons, histamine selectively increased by up to tenfold the amplitude of the component of synaptic transmission that was mediated by N-methyl-D-aspartate (NMDA) receptors. Spontaneous miniature synaptic currents and the current elicited by applied NMDA also were enhanced, indicating that the histamine effect was expressed primarily postsynaptically. These results suggest that histamine may modulate processes involving NMDA receptors, such as the induction of long-term potentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bekkers, J M -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):104-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, John Curtin School of Medical Research, Australian National Univresity, Canberra, ACT.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8391168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cells, Cultured ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Hippocampus/cytology/drug effects/*physiology ; Histamine/*pharmacology ; Ion Channel Gating/drug effects ; N-Methylaspartate/*metabolism/pharmacology ; Rats ; Receptors, Histamine/physiology ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology ; Synaptic Transmission/*drug effects ; Virulence Factors, Bordetella/pharmacology
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    Methylation and imprinting: from host defense to gene regulation? (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barlow, D P -- New York, N.Y. -- Science. 1993 Apr 16;260(5106):309-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology, Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8469984" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/genetics/*metabolism ; *Dosage Compensation, Genetic ; Embryo, Mammalian/metabolism ; Fathers ; Female ; *Gene Expression Regulation ; Insulin-Like Growth Factor II/genetics ; Male ; Methylation ; Mice ; Models, Genetic ; Mothers ; Oocytes/metabolism ; Receptor, IGF Type 2/genetics ; Spermatozoa/metabolism
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    Complexes of Ras.GTP with Raf-1 and mitogen-activated protein kinase kinase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-11
    Description: The guanosine triphosphate (GTP)-binding protein Ras functions in regulating growth and differentiation; however, little is known about the protein interactions that bring about its biological activity. Wild-type Ras or mutant forms of Ras were covalently attached to an insoluble matrix and then used to examine the interaction of signaling proteins with Ras. Forms of Ras activated either by mutation (Gly12Val) or by binding of the GTP analog, guanylyl-imidodiphosphate (GMP-PNP) interacted specifically with Raf-1 whereas an effector domain mutant, Ile36Ala, failed to interact with Raf-1. Mitogen-activated protein kinase (MAP kinase) activity was only associated with activated forms of Ras. The specific interaction of activated Ras with active MAP kinase kinase (MAPKK) was confirmed by direct assays. Thus the forming of complexes containing MAPKK activity and Raf-1 protein are dependent upon the activity of Ras.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moodie, S A -- Willumsen, B M -- Weber, M J -- Wolfman, A -- CA 39076/CA/NCI NIH HHS/ -- CA 40042/CA/NCI NIH HHS/ -- GM 41220/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Jun 11;260(5114):1658-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Cleveland Clinic Foundation, OH 44106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8503013" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Guanosine Triphosphate/*metabolism ; Guanylyl Imidodiphosphate/metabolism ; In Vitro Techniques ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase Kinases ; Mutation ; Phosphorylation ; Protein Binding ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Proto-Oncogene Proteins p21(ras)/*metabolism ; Rats ; Signal Transduction/physiology
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    The missing AIDS science (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leccese, A P -- New York, N.Y. -- Science. 1993 Aug 6;261(5122):665.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8204122" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*prevention & control ; Adolescent ; Adult ; Female ; Humans ; Male ; Risk-Taking ; *Sexual Behavior ; *Street Drugs ; *Substance-Related Disorders
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    GABA-activated chloride channels in secretory nerve endings (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-01-22
    Description: Neurotransmitters acting on presynaptic terminals regulate synaptic transmission and plasticity. Because of the difficulty of direct electrophysiological recording from small presynaptic terminals, little is known about the ion channels that mediate these actions or about the mechanisms by which transmitter secretion is altered. The patch-clamp technique is used to show that the predominant inhibitory presynaptic neurotransmitter, gamma-aminobutyric acid (GABA), activates a GABAA receptor and gates a chloride channel in the membranes of peptidergic nerve terminals of the posterior pituitary. The opening of a chloride channel by GABA weakly depolarizes the nerve terminal membrane and blocks action potentials. In this way, GABA limits secretion by retarding the spread of excitation into the terminal arborization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, S J -- Jackson, M B -- NS30016/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 22;259(5094):531-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Wisconsin Medical School, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8380942" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicuculline/pharmacology ; Chlordiazepoxide/pharmacology ; Chloride Channels ; Chlorides/*metabolism ; GABA-A Receptor Antagonists ; Male ; Membrane Potentials/drug effects ; Membrane Proteins/drug effects/*physiology ; Muscimol/pharmacology ; Nerve Endings/drug effects/*physiology ; Picrotoxin/pharmacology ; Pituitary Gland, Posterior/drug effects/*physiology ; Rats ; Receptors, GABA-A/*physiology ; gamma-Aminobutyric Acid/*pharmacology
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    Association between brain temperature and dentate field potentials in exploring and swimming rats (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-02-26
    Description: Attempts to correlate behavioral learning with cellular changes, such as increased synaptic efficacy, have often relied on increased extracellular potentials as an index of enhanced synaptic strength. A recent example is the enlarged excitatory field potentials in the dentate gyrus of rats that are learning spatial relations by exploration. The altered hippocampal field potentials do not reflect learning-specific cellular changes but result from a concomitant rise in brain temperature that is caused by the associated muscular effort. Enhanced dentate field excitatory potentials followed both passive and active heating and were linearly related to the brain temperature. These temperature-related effects may mask any learning-induced changes in field potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moser, E -- Mathiesen, I -- Andersen, P -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1324-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, University of Oslo, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8446900" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/physiology ; Body Temperature ; Cerebellar Nuclei/*physiology ; Hippocampus/*physiology ; Male ; Membrane Potentials ; Physical Exertion ; Rats ; Swimming/physiology
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    Mechanism-based inactivation of prostatic acid phosphatase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-26
    Description: Protein phosphatases play important roles in the regulation of cell growth and metabolism, yet little is known about their enzymatic mechanism. By extrapolation from data on inhibitors of other types of hydrolases, an inhibitor of prostatic acid phosphatase was designed that is likely to function as a mechanism-based phosphotyrosine phosphatase inactivator. This molecule, 4-(fluoromethyl)phenyl phosphate, represents a useful paradigm for the design of potent and specific phosphatase inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, J K -- Widlanski, T S -- R01 GM47918-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Nov 26;262(5138):1451-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Indiana University, Bloomington 47405.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8248785" target="_blank"〉PubMed〈/a〉
    Keywords: Acid Phosphatase/*antagonists & inhibitors/metabolism ; Alkylation ; Binding Sites ; Drug Design ; Humans ; Hydrolysis ; Kinetics ; Male ; Organophosphorus Compounds/metabolism/*pharmacology ; Prostate/*enzymology
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    Rat annexin V crystal structure: Ca(2+)-induced conformational changes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-03
    Description: Annexins are a family of calcium- and phospholipid-binding proteins implicated in mediating membrane-related processes such as secretion, signal transduction, and ion channel activity. The crystal structure of rat annexin V was solved to 1.9 angstrom resolution by multiple isomorphous replacement. Unlike previously solved annexin V structures, all four domains bound calcium in this structure. Calcium binding in the third domain induced a large relocation of the calcium-binding loop regions, exposing the single tryptophan residue to the solvent. These alterations in annexin V suggest a role for domain 3 in calcium-triggered interaction with phospholipid membranes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Concha, N O -- Head, J F -- Kaetzel, M A -- Dedman, J R -- Seaton, B A -- R01-DK-41740/DK/NIDDK NIH HHS/ -- R01-NS-20357/NS/NINDS NIH HHS/ -- R29-GM-44554/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 3;261(5126):1321-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Boston University School of Medicine, MA 02118.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8362244" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Annexin A5/*chemistry/metabolism ; Binding Sites ; Calcium/*metabolism ; Computer Graphics ; Crystallization ; Humans ; Hydrogen Bonding ; Molecular Sequence Data ; Protein Conformation ; Rats ; Sequence Alignment ; Tryptophan/chemistry ; X-Ray Diffraction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Nitric oxide and carbon monoxide produce activity-dependent long-term synaptic enhancement in hippocampus (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: Nitric oxide (NO) and carbon monoxide (CO) may act as retrograde messages for long-term potentiation (LTP) in the hippocampus. Zinc protoporphyrin IX, an inhibitor of the enzyme that produces CO, blocked induction of LTP in the CA1 region of hippocampal slices. Application of either NO or CO to slices produced a rapid and long-lasting increase in the size of evoked synaptic potentials if, and only if, the application occurred at the same time as weak tetanic stimulation. This long-term enhancement was spatially restricted to synapses from active presynaptic fibers and appeared to involve mechanisms utilized by LTP, occluding the subsequent induction of LTP by strong tetanic stimulation. The enhancement by NO and CO was not blocked by an N-methyl-D-aspartate (NMDA) receptor blocker, suggesting that NO and CO act downstream from the NMDA receptor. Also, CO produced long-term enhancement when paired with low-frequency stimulation. These results are consistent with the hypothesis that NO and CO, either alone or in combination, serve as retrograde messages that produce activity-dependent presynaptic enhancement during LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhuo, M -- Small, S A -- Kandel, E R -- Hawkins, R D -- AG08702/AG/NIA NIH HHS/ -- MH45923/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1946-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, New York, NY.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8100368" target="_blank"〉PubMed〈/a〉
    Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione ; Animals ; Carbon Monoxide/*pharmacology ; Electric Stimulation ; Guinea Pigs ; Hippocampus/drug effects/*physiology ; In Vitro Techniques ; Male ; Membrane Potentials/drug effects ; Nitric Oxide/*pharmacology ; Protoporphyrins/pharmacology ; Quinoxalines/pharmacology ; Signal Transduction/drug effects ; Synapses/drug effects/*physiology
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    Delivery of Na+,K(+)-ATPase in polarized epithelial cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zurzolo, C -- Rodriguez-Boulan, E -- GM 34107/GM/NIGMS NIH HHS/ -- R01 GM034107/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 23;260(5107):550-2; author reply 554-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8386394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/*enzymology ; *Cell Polarity ; Epithelial Cells ; Rats ; *Sodium-Potassium-Exchanging ATPase/*metabolism
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    Cure of xenografted human carcinomas by BR96-doxorubicin immunoconjugates (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-09
    Description: Immunoconjugates (BR96-DOX) were prepared between chimeric monoclonal antibody BR96 and the anticancer drug doxorubicin. The monoclonal antibody binds an antigen related to Lewis Y that is abundantly expressed at the surface of cells from many human carcinomas; it has a high degree of tumor selectivity and is internalized after binding. BR96-DOX induced complete regressions and cures of xenografted human lung, breast, and colon carcinomas growing subcutaneously in athymic mice and cured 70 percent of mice bearing extensive metastases of a human lung carcinoma. Also, BR96-DOX cured 94 percent of athymic rats with subcutaneous human lung carcinoma, even though the rats, like humans and in contrast to mice, expressed the BR96 target antigen in normal tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trail, P A -- Willner, D -- Lasch, S J -- Henderson, A J -- Hofstead, S -- Casazza, A M -- Firestone, R A -- Hellstrom, I -- Hellstrom, K E -- New York, N.Y. -- Science. 1993 Jul 9;261(5118):212-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, NJ 08543.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8327892" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/administration & dosage/immunology/*therapeutic use ; Antigens, Neoplasm/immunology ; Antigens, Surface/immunology ; Breast Neoplasms/drug therapy ; Colonic Neoplasms/drug therapy ; Doxorubicin/administration & dosage/*therapeutic use ; Humans ; Immunotoxins/administration & dosage/*therapeutic use ; Lung Neoplasms/drug therapy ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms, Experimental/*drug therapy ; Rats ; Rats, Nude
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    To Be2+ or not to Be2+: immunogenetics and occupational exposure (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newman, L S -- ES00173/ES/NIEHS NIH HHS/ -- ES06538/ES/NIEHS NIH HHS/ -- HL273353/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 8;262(5131):197-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Occupational and Environmental Medicine Division, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8105535" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen-Presenting Cells/immunology ; Berylliosis/*etiology/genetics/immunology/prevention & control ; Beryllium/*adverse effects/immunology ; Female ; Genes, MHC Class II ; Genetic Markers ; Glutamates ; Glutamic Acid ; HLA-DP Antigens/chemistry/*genetics/immunology ; Humans ; Male ; *Occupational Exposure ; Risk Factors ; T-Lymphocytes, Helper-Inducer/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Optical time-of-flight and absorbance imaging of biologic media (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: Imaging the interior of living bodies with light may assist in the diagnosis and treatment of a number of clinical problems, which include the early detection of tumors and hypoxic cerebral injury. An existing picosecond time-of-flight and absorbance (TOFA) optical system has been used to image a model biologic system and a rat. Model measurements confirmed TOFA principles in systems with a high degree of photon scattering; rat images, which were constructed from the variable time delays experienced by a fixed fraction of early-arriving transmitted photons, revealed identifiable internal structure. A combination of light-based quantitative measurement and TOFA localization may have applications in continuous, noninvasive monitoring for structural imaging and spatial chemometric analysis in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benaron, D A -- Stevenson, D K -- RR-00081/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1463-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Stanford University School of Medicine, Palo Alto, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8451643" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Light ; Models, Theoretical ; Radiation ; Rats ; Spectrophotometry/instrumentation/*methods ; Time Factors
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    Evidence of genetic heterogeneity in the long QT syndrome (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benhorin, J -- Kalman, Y M -- Medina, A -- Towbin, J -- Rave-Harel, N -- Dyer, T D -- Blangero, J -- MacCluer, J W -- Kerem, B S -- 5R01-HL-33843/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1960-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8316839" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Alleles ; Child ; Female ; Genetic Linkage ; Humans ; Long QT Syndrome/*genetics ; Male ; Pedigree ; Phenotype
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    Interaction between transcription regulatory regions of prolactin chromatin (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-09
    Description: The regulation of transcription requires complex interactions between proteins bound to DNA sequences that are often separated by hundreds of base pairs. As demonstrated by a nuclear ligation assay, the distal enhancer and the proximal promoter regions of the rat prolactin gene were found to be juxtaposed. By acting through its receptor bound to the distal enhancer, estrogen stimulated the interaction between the distal and proximal regulatory regions two- to threefold compared to control values. Thus, the chromatin structure of the prolactin gene may facilitate the occurrence of protein-protein interactions between transcription factors bound to widely separated regulatory elements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cullen, K E -- Kladde, M P -- Seyfred, M A -- DK42731/DK/NIDDK NIH HHS/ -- T32HD07048/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 9;261(5118):203-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Vanderbilt University, Nashville, TN 37235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8327891" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Nucleus/metabolism ; Chromatin/*chemistry/metabolism ; DNA/chemistry/metabolism ; Deoxyribonucleases, Type II Site-Specific ; *Enhancer Elements, Genetic ; Estrogens/metabolism ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction ; Prolactin/*genetics ; *Promoter Regions, Genetic ; Protein Conformation ; Protein Folding ; Rats ; Receptors, Estrogen/metabolism ; Regulatory Sequences, Nucleic Acid ; *Transcription, Genetic
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    Nocturnal researchers tune their ears to our ancestors (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culotta, E -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):30-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8316854" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Communication ; Animals ; *Behavior, Animal ; Female ; Homing Behavior ; Male ; *Strepsirhini ; Vocalization, Animal
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    Evolutionists take the long view on sex and violence (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1993 Aug 20;261(5124):987-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8351524" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal ; *Biological Evolution ; Child ; *Child Abuse ; Female ; *Homicide ; Humans ; Male ; *Parents ; *Warfare
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    Where are 'new' diseases born? (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-08-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1993 Aug 6;261(5122):680-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342035" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brazil/epidemiology ; Disease Vectors ; Ecology ; Epidemiologic Methods ; Female ; Humans ; Infection/*epidemiology/transmission ; Male ; Papua New Guinea/epidemiology ; *Trees ; Tropical Medicine
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    Biologists visit New Orleans (under an assumed name) (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Travis, J -- New York, N.Y. -- Science. 1993 Apr 9;260(5105):162-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8469970" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/drug effects ; Animals ; Colonic Neoplasms/*genetics ; Flumazenil/*pharmacology ; *Genes, DCC ; Humans ; Memory/*drug effects ; Rats ; Societies, Scientific/organization & administration
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    The search for liver stem cells picks up (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Travis, J -- New York, N.Y. -- Science. 1993 Mar 26;259(5103):1829.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456311" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Humans ; Liver/*cytology ; Rats ; Stem Cells/*cytology
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    AIDS theories (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-01-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curtis, T -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):14.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418488" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Acquired Immunodeficiency Syndrome/immunology/*transmission ; Animals ; Cells, Cultured ; *Hiv-1 ; Haplorhini ; Humans ; Kidney ; Male
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    Cytoskeletal role in the contractile dysfunction of hypertrophied myocardium (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-04-30
    Description: Cardiac hypertrophy in response to systolic pressure loading frequently results in contractile dysfunction of unknown cause. In the present study, pressure loading increased the microtubule component of the cardiac muscle cell cytoskeleton, which was responsible for the cellular contractile dysfunction observed. The linked microtubule and contractile abnormalities were persistent and thus may have significance for the deterioration of initially compensatory cardiac hypertrophy into congestive heart failure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsutsui, H -- Ishihara, K -- Cooper, G 4th -- HL37196/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):682-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Medical University of South Carolina, Charleston.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8097594" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/drug effects/physiology ; Animals ; Cardiomegaly/pathology/*physiopathology ; Cats ; Colchicine/pharmacology ; Cytochalasin D/pharmacology ; Desmin/physiology ; Female ; Heart Septal Defects, Atrial/physiopathology ; Intermediate Filaments/drug effects/physiology ; Male ; Microtubules/drug effects/pathology/*physiology ; *Myocardial Contraction ; Myocardium/*pathology ; Paclitaxel/pharmacology ; Pressure ; Sarcomeres/drug effects/physiology ; Ventricular Function, Right
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    Interspecific and intraspecific horizontal transfer of Wolbachia in Drosophila (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-06-18
    Description: Cytoplasmic incompatibility (CI) in Drosophila simulans is related to infection of the germ line by a rickettsial endosymbiont (genus Wolbachia). Wolbachia were transferred by microinjection of egg cytoplasm into uninfected eggs of both D. simulans and D. melanogaster to generate infected populations. Transinfected strains of D. melanogaster with lower densities of Wolbachia than the naturally infected D. simulans strain did not express high levels of CI. However, transinfected D. melanogaster egg cytoplasm, transferred back into D. simulans, generated infected populations that expressed CI at levels near those of the naturally infected strain. A transinfected D. melanogaster line selected for increased levels of CI expression also displayed increased symbiont densities. These data suggest that a threshold level of infection is required for normal expression of CI and that host factors help determine the density of the symbiont in the host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyle, L -- O'Neill, S L -- Robertson, H M -- Karr, T L -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1796-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Illinois, Urbana 61801.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8511587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytoplasm/microbiology/physiology ; Drosophila/*microbiology/physiology ; Drosophila melanogaster/*microbiology/physiology ; Female ; Male ; Microinjections ; Microscopy ; Ovum/microbiology/physiology ; Rickettsiaceae/*physiology
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    Hantavirus outbreak yields to PCR (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-11-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):832, 834-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235602" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bunyaviridae Infections/epidemiology/*microbiology/therapy/transmission ; Disease Outbreaks ; Disease Reservoirs ; Disease Vectors ; Female ; Genome, Viral ; Hantavirus/*genetics/isolation & purification/pathogenicity ; Humans ; Lung Diseases/epidemiology/*microbiology/therapy ; Male ; Peromyscus/microbiology ; *Polymerase Chain Reaction ; Rodent Control ; Southwestern United States/epidemiology ; United States/epidemiology
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    Mammalian locomotor-respiratory integration: implications for diaphragmatic and pulmonary design (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-08
    Description: Diaphragmatic function and intrapulmonary respiratory flow in running mammals were found to differ substantially from the corresponding conditions known in resting mammals. In trotting dogs, orbital oscillations of the diaphragm were driven by inertial displacements of the viscera induced by locomotion. In turn, oscillations of the visceral mass drove pulmonary ventilation independent of diaphragmatic contractions, which primarily served to modulate visceral kinetics. Visceral displacements and loading of the anterior chest wall by the forelimbs are among the factors that contribute to an asynchronous ventilation of the lungs and interlobar gas recycling. Basic features of mammalian respiratory design, including the structure of the diaphragm and lobation of the lungs, appear to reflect the mechanical requirements of locomotor-respiratory integration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bramble, D M -- Jenkins, F A Jr -- S07 RR07092/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 8;262(5131):235-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Utah, Salt Lake City 84112.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cineradiography ; Diaphragm/anatomy & histology/*physiology ; Dogs ; Female ; Locomotion/*physiology ; Lung/anatomy & histology/*physiology/radiography ; Male ; Models, Biological ; Muscle Contraction ; Radiography, Thoracic ; Respiratory Mechanics/*physiology
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    Action of antiulcer drugs (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Panula, P -- Wasowicz, K -- New York, N.Y. -- Science. 1993 Nov 26;262(5138):1454; author reply 1454-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8248787" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Ulcer Agents/pharmacology ; Gastric Mucosa/*chemistry ; Histidine Decarboxylase/analysis ; Macrophages/chemistry ; Oligonucleotide Probes ; Rats ; Receptors, Cell Surface/analysis ; Receptors, Histamine H2/*analysis
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    Crystal structure of domains 3 and 4 of rat CD4: relation to the NH2-terminal domains (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-14
    Description: The CD4 antigen is a membrane glycoprotein of T lymphocytes that interacts with major histocompatibility complex class II antigens and is also a receptor for the human immunodeficiency virus. the extracellular portion of CD4 is predicted to fold into four immunoglobulin-like domains. The crystal structure of the third and fourth domains of rat CD4 was solved at 2.8 angstrom resolution and shows that both domains have immunoglobulin folds. Domain 3, however, lacks the disulfide between the beta sheets; this results in an expansion of the domain. There is a difference of 30 degrees in the orientation between domains 3 and 4 when compared with domains 1 and 2. The two CD4 fragment structures provide a basis from which models of the overall receptor can be proposed. These models suggest an extended structure comprising two rigid portions joined by a short and possibly flexible linker region.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brady, R L -- Dodson, E J -- Dodson, G G -- Lange, G -- Davis, S J -- Williams, A F -- Barclay, A N -- New York, N.Y. -- Science. 1993 May 14;260(5110):979-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of York, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493535" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD4/*chemistry ; Crystallization ; Humans ; Models, Molecular ; Molecular Sequence Data ; Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Rats ; Sequence Alignment ; X-Ray Diffraction
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    Released form of CNTF receptor alpha component as a soluble mediator of CNTF responses (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: The alpha component of the receptor for ciliary neurotrophic factor (CNTF) differs from other known growth factor receptors in that it is anchored to cell membranes by a glycosylphosphatidylinositol linkage. One possible function of this type of linkage is to allow for the regulated release of this receptor component. Cell lines not normally responsive to CNTF responded to treatment with a combination of CNTF and a soluble form of the CNTF alpha receptor component. These findings not only demonstrate that the CNTF receptor alpha chain is a required component of the functional CNTF receptor complex but also reveal that it can function in soluble form as part of a heterodimeric ligand. Potential physiological roles for the soluble CNTF receptor are suggested by its presence in cerebrospinal fluid and by its release from skeletal muscle in response to peripheral nerve injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S -- Aldrich, T H -- Ip, N Y -- Stahl, N -- Scherer, S -- Farruggella, T -- DiStefano, P S -- Curtis, R -- Panayotatos, N -- Gascan, H -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1736-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, Inc., Tarrytown, NY 10591.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7681218" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cell Membrane/metabolism ; Ciliary Neurotrophic Factor ; Cloning, Molecular ; Gene Expression ; Glycosylphosphatidylinositols/metabolism ; Growth Inhibitors/pharmacology ; Hematopoietic Stem Cells/cytology/drug effects ; Humans ; Interleukin-6/pharmacology ; Leukemia Inhibitory Factor ; Lymphokines/pharmacology ; Mice ; Muscle Denervation ; Muscles/innervation/metabolism ; Nerve Tissue Proteins/*pharmacology ; Phosphatidylinositol Diacylglycerol-Lyase ; Phosphoric Diester Hydrolases/metabolism ; Phosphotyrosine ; RNA, Messenger/genetics ; Rats ; Receptor, Ciliary Neurotrophic Factor ; Receptors, Cell Surface/chemistry/*physiology ; Signal Transduction/physiology ; Tumor Cells, Cultured ; Tyrosine/analogs & derivatives/metabolism
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    Effects of oral administration of type II collagen on rheumatoid arthritis (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-24
    Description: Rheumatoid arthritis is an inflammatory synovial disease thought to involve T cells reacting to an antigen within the joint. Type II collagen is the major protein in articular cartilage and is a potential autoantigen in this disease. Oral tolerization to autoantigens suppresses animal models of T cell-mediated autoimmune disease, including two models of rheumatoid arthritis. In this randomized, double-blind trial involving 60 patients with severe, active rheumatoid arthritis, a decrease in the number of swollen joints and tender joints occurred in subjects fed chicken type II collagen for 3 months but not in those that received a placebo. Four patients in the collagen group had complete remission of the disease. No side effects were evident. These data demonstrate clinical efficacy of an oral tolerization approach for rheumatoid arthritis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trentham, D E -- Dynesius-Trentham, R A -- Orav, E J -- Combitchi, D -- Lorenzo, C -- Sewell, K L -- Hafler, D A -- Weiner, H L -- AG00294/AG/NIA NIH HHS/ -- MO1 RR01032/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 24;261(5129):1727-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Beth Israel Hospital, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8378772" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Adult ; Aged ; Arthritis, Rheumatoid/*drug therapy/immunology ; Autoimmune Diseases/*drug therapy/immunology ; Collagen/*administration & dosage/adverse effects/therapeutic use ; Double-Blind Method ; Female ; Humans ; Immune Tolerance ; Male ; Middle Aged ; Placebo Effect ; T-Lymphocytes/immunology
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    Development of mature CD8+ thymocytes: selection rather than instruction? (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-13
    Description: The role of major histocompatibility complex (MHC) molecules in T cell differentiation was investigated by comparison of thymocyte subpopulations in wild-type mice and beta 2-microglobulin (beta 2M) mutant mice deficient in MHC class I expression and mature CD8+ cells. On the basis of surface markers, glucocorticoid resistance, in vitro differentiation capacity, and absence in beta 2 M-l- mice, CD4intermediateCD8hi cells with high expression of alpha beta T cell receptor (TCR alpha beta) were identified as having been positively selected by MHC class I for development into mature CD8+ T cells. Activated CD4intCD8hi cells bearing intermediate rather than high amounts of TCR were present in both wild-type and beta 2M-l- animals. These data suggest that recognition of MHC class I molecules is required for full maturation to CD8+ T cells, but not for receptor-initiated commitment to the CD8+ lineage, consistent with a stochastic (selection) model of thymocyte development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Meerwijk, J P -- Germain, R N -- New York, N.Y. -- Science. 1993 Aug 13;261(5123):911-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Biology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8102208" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/analysis ; Antigens, CD8/*analysis ; CD4-Positive T-Lymphocytes/cytology/immunology ; Cell Differentiation ; Dexamethasone/pharmacology ; Histocompatibility Antigens Class I/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Phenotype ; Receptors, Antigen, T-Cell, alpha-beta/*analysis ; T-Lymphocyte Subsets/cytology/drug effects/*immunology
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    Beta-adrenergic receptor kinase-2 and beta-arrestin-2 as mediators of odorant-induced desensitization (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: beta-Adrenergic receptor kinase (beta ARK) and beta-arrestin function in the homologous or agonist-activated desensitization of G protein-coupled receptors. The isoforms beta ARK-2 and beta-arrestin-2 are highly enriched in and localized to the dendritic knobs and cilia of the olfactory receptor neurons where the initial events of olfactory signal transduction occur. Odorants induce a rapid and transient elevation of adenosine 3',5'-monophosphate (cAMP), which activates a nonspecific cation channel and produces membrane depolarization. Preincubation of rat olfactory cilia with antibodies raised against beta ARK-2 and beta-arrestin-2 increased the odorant-induced elevation of cAMP and attenuated desensitization. These results suggest that beta ARK-2 and beta-arrestin-2 mediate agonist-dependent desensitization in olfaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, T M -- Arriza, J L -- Jaworsky, D E -- Borisy, F F -- Attramadal, H -- Lefkowitz, R J -- Ronnett, G V -- NS 01578-01/NS/NINDS NIH HHS/ -- NS-02131/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):825-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins Medical Institutions, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8381559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*metabolism ; *Arrestins ; Cells, Cultured ; Cyclic AMP/metabolism ; *Cyclic AMP-Dependent Protein Kinases ; Cytosol/metabolism ; Dendrites/physiology ; Eye Proteins/*metabolism ; G-Protein-Coupled Receptor Kinase 2 ; GTP-Binding Proteins/*metabolism ; Isoenzymes/metabolism ; Male ; Mechanoreceptors/*physiology ; Neurons/*physiology ; *Odors ; Olfactory Bulb/*physiology ; Protein Kinases/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta/*physiology ; Signal Transduction ; *Smell ; Testis/physiology ; Turbinates/*physiology ; beta-Adrenergic Receptor Kinases
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    Proliferation of human smooth muscle cells promoted by lipoprotein(a) (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-11
    Description: Elevated blood concentrations of lipoprotein(a) [Lp(a)] and its constituent, apolipoprotein(a) [apo(a)], constitute a major risk factor for atherosclerosis, but their physiological activities remain obscure. Lp(a) and purified apo(a) stimulated the growth of human smooth muscle cells in culture. This effect resulted from inhibition of plasminogen activation, and consequently the activation by plasmin of latent transforming growth factor-beta, which is an inhibitor of smooth muscle cell growth. Because smooth muscle proliferation is one of the hallmarks of atherosclerotic lesions, these results point to a plausible mechanism for the atherogenic activity of Lp(a).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grainger, D J -- Kirschenlohr, H L -- Metcalfe, J C -- Weissberg, P L -- Wade, D P -- Lawn, R M -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Jun 11;260(5114):1655-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8503012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins/physiology ; Apoprotein(a) ; Cell Division/drug effects/physiology ; Cells, Cultured ; Fibrinolysin/physiology ; Humans ; Lipoprotein(a)/*physiology ; Muscle, Smooth, Vascular/*cytology/metabolism ; Plasminogen Activators/metabolism ; Rats ; Tamoxifen/pharmacology ; Transforming Growth Factor beta/physiology
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    Arrestin function in inactivation of G protein-coupled receptor rhodopsin in vivo (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: Arrestins have been implicated in the regulation of many G protein-coupled receptor signaling cascades. Mutations in two Drosophila photoreceptor-specific arrestin genes, arrestin 1 and arrestin 2, were generated. Analysis of the light response in these mutants shows that the Arr1 and Arr2 proteins are mediators of rhodopsin inactivation and are essential for the termination of the phototransduction cascade in vivo. The saturation of arrestin function by an excess of activated rhodopsin is responsible for a continuously activated state of the photoreceptors known as the prolonged depolarized afterpotential. In the absence of arrestins, photoreceptors undergo light-dependent retinal degeneration as a result of the continued activity of the phototransduction cascade. These results demonstrate the fundamental requirement for members of the arrestin protein family in the regulation of G protein-coupled receptors and signaling cascades in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dolph, P J -- Ranganathan, R -- Colley, N J -- Hardy, R W -- Socolich, M -- Zuker, C S -- R01 EY008768/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1910-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, La Jolla, CA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8316831" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; *Arrestins ; Drosophila ; Drosophila Proteins ; Eye Proteins/genetics/*physiology ; Female ; GTP-Binding Proteins/*metabolism ; Genes, Insect ; Kinetics ; Male ; Molecular Sequence Data ; Mutation ; Phosphoproteins/genetics/*physiology ; Photic Stimulation ; Photoreceptor Cells/cytology/*physiology ; Rhodopsin/analogs & derivatives/*metabolism
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    Genetic mapping of a locus predisposing to human colorectal cancer (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-07
    Description: Genetic linkage analysis was used to determine whether a specific chromosomal locus could be implicated in families with a history of early onset cancer but with no other unique features. Close linkage of disease to anonymous microsatellite markers on chromosome 2 was demonstrated in two large kindreds. The pairwise lod scores for linkage to marker D2S123 in these kindreds were 6.39 and 1.45 at zero recombination, and multipoint linkage with flanking markers resulted in lod scores of 6.47 and 6.01. These results prove the existence of a genetically determined predisposition to colorectal cancer that has important ramifications for understanding and preventing this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peltomaki, P -- Aaltonen, L A -- Sistonen, P -- Pylkkanen, L -- Mecklin, J P -- Jarvinen, H -- Green, J S -- Jass, J R -- Weber, J L -- Leach, F S -- CA 35494/CA/NCI NIH HHS/ -- CA 47527/CA/NCI NIH HHS/ -- HG 00248/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 7;260(5109):810-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Genetics, University of Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484120" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Mapping ; *Chromosomes, Human, Pair 2 ; Colonic Neoplasms/*genetics ; Colorectal Neoplasms/*genetics ; DNA, Satellite/genetics ; Disease Susceptibility ; Female ; *Genes ; Genetic Markers ; Humans ; Male ; Pedigree ; Rectal Neoplasms/genetics
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    Identification of a whitefly species by genomic and behavioral studies (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: An introduced whitefly species, responsible for over a half billion dollars in damage to U.S. agricultural production in 1991, is morphologically indistinguishable from Bemisia tabaci (Gennadius). However, with the use of polymerase chain reaction-based DNA differentiation tests, allozymic frequency analyses, crossing experiments, and mating behavior studies, the introduced whitefly is found to be a distinct species. Recognition of this new species, the silverleaf whitefly, is critical in the search for management options.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perring, T M -- Cooper, A D -- Rodriguez, R J -- Farrar, C A -- Bellows, T S Jr -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):74-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Entomology, University of California, Riverside 92521.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418497" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; Crosses, Genetic ; DNA/genetics ; Diptera/*classification/genetics/*physiology ; Enzymes/genetics ; Female ; Genetic Linkage ; Male ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Sexual Behavior, Animal ; United States
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    Relation of phenotype evolution of HIV-1 to envelope V2 configuration (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-04
    Description: Biological variability of human immunodeficiency virus type-1 (HIV-1) is involved in the pathogenesis of acquired immunodeficiency syndrome (AIDS). Syncytium-inducing (SI) HIV-1 variants emerge in 50 percent of infected individuals during infection, preceding accelerated CD4+ T cell loss and rapid progression to AIDS. The V1 to V2 and V3 region of the viral envelope glycoprotein gp120 contained the major determinants of SI capacity. The configuration of a hypervariable locus in the V2 domain appeared to be predictive for non-SI to SI phenotype conversion. Early prediction of HIV-1 phenotype evolution may be useful for clinical monitoring and treatment of asymptomatic infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Groenink, M -- Fouchier, R A -- Broersen, S -- Baker, C H -- Koot, M -- van't Wout, A B -- Huisman, H G -- Miedema, F -- Tersmette, M -- Schuitemaker, H -- New York, N.Y. -- Science. 1993 Jun 4;260(5113):1513-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Viro-Immunology, Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8502996" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/microbiology ; Amino Acid Sequence ; Base Sequence ; Biological Evolution ; Consensus Sequence ; Genetic Variation ; Giant Cells/microbiology ; HIV Envelope Protein gp120/*chemistry ; HIV Seropositivity/microbiology ; HIV-1/*chemistry/*genetics/pathogenicity ; Humans ; Male ; Molecular Sequence Data ; Phenotype ; Protein Conformation ; Recombination, Genetic
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    Antisense gene inhibition by oligonucleotides containing C-5 propyne pyrimidines (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-04
    Description: Phosphorothioate oligodeoxynucleotides containing the C-5 propyne analogs of uridine and cytidine bind RNA with high affinity and are potent antisense inhibitors of gene expression. In a cellular assay, gene-specific antisense inhibition occurred at nanomolar concentrations of oligonucleotide, was dose-dependent and exquisitely sensitive to sequence mismatches, and was correlated with the melting temperature and length of oligonucleotide. Activity was independent of RNA target site and cell type but was detectable only when the oligonucleotides were microinjected or delivered with cell-permeabilizing agents. These oligonucleotides may have important applications in therapy and in studies of gene function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wagner, R W -- Matteucci, M D -- Lewis, J G -- Gutierrez, A J -- Moulds, C -- Froehler, B C -- New York, N.Y. -- Science. 1993 Jun 4;260(5113):1510-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gilead Sciences, Inc., Foster City, CA 94404.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7684856" target="_blank"〉PubMed〈/a〉
    Keywords: Alkynes/pharmacology ; Animals ; Base Sequence ; Cell Line ; Cercopithecus aethiops ; Humans ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacokinetics/*pharmacology ; Pyrimidine Nucleotides/pharmacokinetics/*pharmacology ; RNA/*drug effects ; Rats ; Thionucleotides/pharmacokinetics/*pharmacology
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    Congress may hang up on AIDS hotline (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1993 Apr 30;260(5108):611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480171" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*prevention & control ; Counseling/*legislation & jurisprudence ; Financing, Government ; *Homosexuality ; Hotlines/*legislation & jurisprudence ; Humans ; Male ; National Institute of Mental Health (U.S.) ; United States
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    Ice man's fungi: discussion rekindled (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Poder, R -- New York, N.Y. -- Science. 1993 Dec 24;262(5142):1956.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8086009" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Freezing ; History, Ancient ; Hominidae/*microbiology ; Humans ; Male ; *Mummies ; Polyporaceae/*isolation & purification
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    Chemorepulsion of axons in the developing mammalian central nervous system (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-02
    Description: During development of the nervous system, distinct populations of nerve cells extend specialized processes, axons and dendrites, over considerable distances to locate their targets. There is strong evidence for two general mechanisms by which these connections are made. The first involves attractive and repulsive interactions, both between cells and between them and their extracellular matrix. The second depends on the release of diffusible chemoattractants by target structures. Evidence is now provided for a mechanism of axon guidance in which diffusible chemorepulsive factors create exclusion zones for developing axons, causing them to turn away from inappropriate territory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pini, A -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):95-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Mammalian Development Unit, London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8316861" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cerebral Cortex/cytology/embryology/physiology ; Contact Inhibition ; Culture Techniques ; Olfactory Bulb/cytology/*embryology/physiology ; Olfactory Pathways/cytology/*embryology/physiology ; Rats ; Telencephalon/cytology/embryology/physiology
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    New Sellafield study poses a puzzle (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kingman, S -- New York, N.Y. -- Science. 1993 Oct 29;262(5134):648-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235581" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; Cluster Analysis ; England/epidemiology ; Fathers ; Humans ; Leukemia, Radiation-Induced/epidemiology ; Male ; Neoplasms, Radiation-Induced/*epidemiology ; *Nuclear Reactors ; *Occupational Exposure
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  • 77
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    Prevention of collagen-induced arthritis with an antibody to gp39, the ligand for CD40 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-03
    Description: The ligand for the CD40 antigen is a 39-kilodalton protein, gp39, expressed on the surface of activated CD4+ T cells and is essential for thymus-dependent humoral immunity. The role of gp39-CD40 interactions in autoimmune disease was investigated in vivo with the use of an antibody that blocks their interactions (anti-gp39). Arthritis induced in mice by immunization with type II collagen was inhibited by anti-gp39. Anti-gp39 blocked the development of joint inflammation, serum antibody titers to collagen, the infiltration of inflammatory cells into the subsynovial tissue, and the erosion of cartilage and bone. Thus, interference with gp39-CD40 interactions may have therapeutic potential in the treatment of autoimmune disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Durie, F H -- Fava, R A -- Foy, T M -- Aruffo, A -- Ledbetter, J A -- Noelle, R J -- AI26296/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 3;261(5126):1328-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Dartmouth Medical School, Lebanon, NH 03756.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7689748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*immunology ; Antigens, CD/*immunology ; Antigens, CD40 ; Antigens, Differentiation, B-Lymphocyte/*immunology ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Arthritis, Experimental/immunology/pathology/prevention & control ; Arthritis, Rheumatoid/immunology/pathology/*prevention & control ; Autoimmune Diseases/immunology/pathology/*prevention & control ; CD40 Ligand ; Collagen/immunology ; Disease Models, Animal ; Immunization ; Immunoglobulin G/blood ; Joints/pathology ; Ligands ; Male ; Membrane Glycoproteins/*immunology ; Mice ; Mice, Inbred DBA
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    Feedback regulation mechanisms for the control of GTP cyclohydrolase I activity (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-04
    Description: Guanosine triphosphate (GTP) cyclohydrolase I, the rate-limiting enzyme in the biosynthesis of tetrahydrobiopterin (BH4), is subject to feedback inhibition by BH4, a cofactor for phenylalanine hydroxylase. Inhibition was found to depend specifically on BH4 and the presence of another protein (p35). The inhibition occurred through BH4-dependent complex formation between p35 protein and GTP cyclohydrolase I. Furthermore, the inhibition was specifically reversed by phenylalanine, and, in conjunction with p35, phenylalanine reduced the cooperativity of GTP cyclohydrolase I. These findings also provide a molecular basis for high plasma BH4 concentrations observed in patients with hyperphenylalaninemia caused by phenylalanine hydroxylase deficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harada, T -- Kagamiyama, H -- Hatakeyama, K -- New York, N.Y. -- Science. 1993 Jun 4;260(5113):1507-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Osaka Medical College, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8502995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Factors/physiology ; Biopterin/analogs & derivatives/physiology ; Chromatography, Gel ; Feedback ; GTP Cyclohydrolase/antagonists & inhibitors/*metabolism ; Humans ; In Vitro Techniques ; Liver/metabolism ; Phenylalanine/physiology ; Phenylalanine Hydroxylase/metabolism ; Protein Binding ; Rats ; Recombinant Proteins/metabolism ; Tissue Extracts
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    Induction of type I diabetes by interferon-alpha in transgenic mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: Type I diabetes is an autoimmune disease involving an interaction between an epigenetic event (possibly a viral infection), the pancreatic beta cells, and the immune system in a genetically susceptible host. The possibility that the type I interferons could mediate this interaction was tested with transgenic mice in which the insulin-producing beta cells expressed an interferon-alpha. These mice developed a hypoinsulinemic diabetes associated with a mixed inflammation centered on the islets. The inflammation and the diabetes were prevented with a neutralizing antibody to the interferon-alpha. Thus, the expression of interferon-alpha by the beta cells could be causal in the development of type I diabetes, which suggests a therapeutic approach to this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stewart, T A -- Hultgren, B -- Huang, X -- Pitts-Meek, S -- Hully, J -- MacLachlan, N J -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1942-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Endocrine Research, Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8100367" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/therapeutic use ; CD4-CD8 Ratio ; CD4-Positive T-Lymphocytes ; Diabetes Mellitus, Type 1/*etiology/immunology/pathology ; Female ; Glucagon/analysis ; Insulin/analysis/blood ; Interferon-alpha/*biosynthesis/immunology ; Islets of Langerhans/immunology/*metabolism/pathology ; Leukocytes, Mononuclear ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neutralization Tests ; Somatostatin/analysis
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  • 80
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    The learning of categories: parallel brain systems for item memory and category knowledge (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-10
    Description: A fundamental question about cognition concerns how knowledge about a category is acquired through encounters with examples of the category. Amnesic patients and control subjects performed similarly at classifying novel patterns according to whether they belonged to the same category as a set of training patterns. In contrast, the amnesic patients were impaired at recognizing which dot patterns had been presented for training. Category learning appears to be independent of declarative (explicit) memory for training instances and independent of the brain structures essential for declarative memory that are damaged in amnesia. Knowledge about categories can be acquired implicitly by cumulating information from multiple examples.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knowlton, B J -- Squire, L R -- MH24600/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 10;262(5140):1747-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Veterans Affairs Medical Center, San Diego, CA 92161.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8259522" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Amnesia/*psychology ; Female ; Humans ; *Learning ; Male ; *Memory ; Middle Aged
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    Thymic selection of cytotoxic T cells independent of CD8 alpha-Lck association (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-17
    Description: The CD8 alpha cytoplasmic domain associates with p56lck, a nonreceptor protein-tyrosine kinase. The biological relevance of CD8 alpha-Lck association in T cell development was tested with transgenic mice generated to express a CD8 alpha molecule with two amino acid substitutions in its cytoplasmic domain, which abolishes the association of CD8 alpha with Lck. The CD8 alpha mutant was analyzed in a CD8-/- background and in the context of the transgenic 2C T cell receptor. The development and function of CD8+ T cells in these mice were apparently normal. Thus, CD8 alpha-Lck association is not necessary for positive selection, negative selection, or CD8-dependent cytotoxic function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, I T -- Limmer, A -- Louie, M C -- Bullock, E D -- Fung-Leung, W P -- Mak, T W -- Loh, D Y -- AI 155322-13/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 17;261(5128):1581-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Genetics, and Molecular Microbiology, 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/8372352" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/metabolism ; Antigens, CD8/immunology/*metabolism ; *Cytotoxicity, Immunologic ; Female ; Genes, MHC Class I ; Lymphocyte Culture Test, Mixed ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Antigen, T-Cell ; T-Lymphocytes, Cytotoxic/*immunology
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    An essential role for protein phosphatases in hippocampal long-term depression (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-20
    Description: The effectiveness of long-term potentiation (LTP) as a mechanism for information storage would be severely limited if processes that decrease synaptic strength did not also exist. In area CA1 of the rat hippocampus, prolonged periods of low-frequency afferent stimulation elicit a long-term depression (LTD) that is specific to the stimulated input. The induction of LTD was blocked by the extracellular application of okadaic acid or calyculin A, two inhibitors of protein phosphatases 1 and 2A. The loading of CA1 cells with microcystin LR, a membrane-impermeable protein phosphatase inhibitor, or calmodulin antagonists also blocked or attenuated LTD. The application of calyculin A after the induction of LTD reversed the synaptic depression, suggesting that phosphatase activity is required for the maintenance of LTD. These findings indicate that the synaptic activation of protein phosphatases plays an important role in the regulation of synaptic transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mulkey, R M -- Herron, C E -- Malenka, R C -- MH00942/MH/NIMH NIH HHS/ -- MH10306/MH/NIMH NIH HHS/ -- MH45334/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1993 Aug 20;261(5124):1051-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of California, San Francisco 94143-0984.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8394601" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calmodulin/metabolism ; Electric Stimulation ; Ethers, Cyclic/pharmacology ; Hippocampus/drug effects/enzymology/*physiology ; Microcystins ; Okadaic Acid ; Oxazoles/pharmacology ; Peptides, Cyclic/pharmacology ; Phosphoprotein Phosphatases/antagonists & inhibitors/*metabolism ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/drug effects/*physiology ; *Synaptic Transmission/drug effects
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    Colocalization of X-linked agammaglobulinemia and X-linked immunodeficiency genes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-16
    Description: Mice that bear the X-linked immunodeficiency (xid) mutation have a B lymphocyte-specific defect resulting in an inability to make antibody responses to polysaccharide antigens. A backcross of 1114 progeny revealed the colocalization of xid with Bruton's agammaglobulinemia tyrosine kinase (btk) gene, which is implicated in the human immune deficiency, X-linked agammaglobulinemia. Mice that carry xid have a missense mutation that alters a highly conserved arginine near the amino-terminus of the btk protein, Btk. Because this region of Btk lies outside any obvious kinase domain, the xid mutation may define another aspect of tyrosine kinase function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, J D -- Sideras, P -- Smith, C I -- Vorechovsky, I -- Chapman, V -- Paul, W E -- GM33160/GM/NIGMS NIH HHS/ -- HG00277/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 16;261(5119):355-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332900" target="_blank"〉PubMed〈/a〉
    Keywords: Agammaglobulinemia/enzymology/*genetics/immunology ; Amino Acid Sequence ; Animals ; B-Lymphocytes/enzymology/immunology ; Base Sequence ; Chromosome Mapping ; Crosses, Genetic ; Female ; *Genes ; Genetic Linkage ; Immunologic Deficiency Syndromes/enzymology/*genetics/immunology ; Male ; Mice ; Mice, Inbred CBA ; Mice, Mutant Strains ; Molecular Sequence Data ; Muridae ; Mutation ; Protein-Tyrosine Kinases/chemistry/*genetics/metabolism ; *X Chromosome
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    The conserved pre-mRNA splicing factor U2AF from Drosophila: requirement for viability (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-22
    Description: The large subunit of the human pre-messenger RNA splicing factor U2 small nuclear ribonucleoprotein auxiliary factor (hU2AF65) is required for spliceosome assembly in vitro. A complementary DNA clone encoding the large subunit of Drosophila U2AF (dU2AF50) has been isolated. The dU2AF50 protein is closely related to its mammalian counterpart and contains three carboxyl-terminal ribonucleoprotein consensus sequence RNA binding domains and an amino-terminal arginine- and serine-rich (R/S) domain. Recombinant dU2AF50 protein complements mammalian splicing extracts depleted of U2AF activity. Germline transformation of Drosophila with the dU2AF50 complementary DNA rescues a lethal mutation, establishing that the dU2AF50 gene is essential for viability. R/S domains have been found in numerous metazoan splicing factors, but their function is unknown. The mutation in Drosophila U2AF will allow in vivo analysis of a conserved R/S domain-containing general splicing factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kanaar, R -- Roche, S E -- Beall, E L -- Green, M R -- Rio, D C -- R01-HD28063/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 22;262(5133):569-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7692602" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Conserved Sequence ; DNA, Complementary ; Drosophila melanogaster/*genetics/growth & development ; Female ; Gene Transfer Techniques ; Genes, Insect ; Genes, Lethal ; In Situ Hybridization ; Male ; Molecular Sequence Data ; Mutation ; *Nuclear Proteins ; RNA/metabolism ; RNA Precursors/*metabolism ; *RNA Splicing ; Recombinant Proteins/metabolism ; Ribonucleoproteins/chemistry/*genetics/metabolism ; Sequence Alignment
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  • 85
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    Retinal degeneration in choroideremia: deficiency of rab geranylgeranyl transferase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-15
    Description: Rab geranylgeranyl transferase (GG transferase) is a two-component enzyme that attaches 20-carbon isoprenoid groups to cysteine residues in Rab proteins, a family of guanosine triphosphate-binding proteins that regulate vesicular traffic. The mutant gene in human choroideremia, an X-linked form of retinal degeneration, encodes a protein that resembles component A of rat Rab GG transferase. Lymphoblasts from choroideremia subjects showed a marked deficiency in the activity of component A, but not component B, of Rab GG transferase. The deficiency was more pronounced when the substrate was Rab3A, a synaptic vesicle protein, than it was when the substrate was Rab1A, a protein of the endoplasmic reticulum. The data imply the existence of multiple component A proteins, one of which is missing in choroideremia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seabra, M C -- Brown, M S -- Goldstein, J L -- HL 20948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):377-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8380507" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Alkyl and Aryl Transferases ; Cell Line, Transformed ; Cells, Cultured ; Choroid/chemistry ; Choroideremia/*genetics ; Female ; GTP-Binding Proteins/analysis/*metabolism ; Gene Expression Regulation, Enzymologic ; Humans ; Lymphocyte Activation ; Male ; Middle Aged ; Mutation ; Nerve Tissue Proteins/analysis/*metabolism ; Photoreceptor Cells/chemistry ; Pigment Epithelium of Eye/chemistry ; Protein Prenylation ; Retina/chemistry ; Substrate Specificity ; Transferases/*deficiency/genetics ; rab1 GTP-Binding Proteins ; rab3 GTP-Binding Proteins
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  • 86
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    Connexin mutations in X-linked Charcot-Marie-Tooth disease (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-24
    Description: X-linked Charcot-Marie-Tooth disease (CMTX) is a form of hereditary neuropathy with demyelination. Recently, this disorder was mapped to chromosome Xq13.1. The gene for the gap junction protein connexin32 is located in the same chromosomal segment, which led to its consideration as a candidate gene for CMTX. With the use of Northern (RNA) blot and immunohistochemistry technique, it was found that connexin32 is normally expressed in myelinated peripheral nerve. Direct sequencing of the connexin32 gene showed seven different mutations in affected persons from eight CMTX families. These findings, a demonstration of inherited defects in a gap junction protein, suggest that connexin32 plays an important role in peripheral nerve.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bergoffen, J -- Scherer, S S -- Wang, S -- Scott, M O -- Bone, L J -- Paul, D L -- Chen, K -- Lensch, M W -- Chance, P F -- Fischbeck, K H -- GM37751/GM/NIGMS NIH HHS/ -- NS01565/NS/NINDS NIH HHS/ -- NS08075/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Dec 24;262(5142):2039-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of Pennsylvania Medical School, Children's Hospital of Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266101" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Charcot-Marie-Tooth Disease/*genetics ; Chromosome Mapping ; Connexins/analysis/*genetics ; Female ; Genetic Linkage ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Nerve Fibers, Myelinated/chemistry ; Nerve Tissue Proteins/analysis ; Peripheral Nerves/chemistry ; Rats ; X Chromosome
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    Rhythmic exocytosis stimulated by GnRH-induced calcium oscillations in rat gonadotropes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-02
    Description: In pituitary gonadotropes, gonadotropin-releasing hormone (GnRH) induces the rhythmic release of Ca2+ from an inositol 1,4,5-trisphosphate (IP3)-sensitive store. Simultaneous measurement of the concentration of cytosolic free Ca2+ ([Ca2+]i) and exocytosis in single identified gonadotropes showed that each elevation of [Ca2+]i induced a burst of exocytosis. These phenomena were largely suppressed by buffering of [Ca2+]i but persisted in the absence of extracellular Ca2+. Activation of voltage-gated Ca2+ channels by brief depolarizations seldom supplied enough Ca2+ for exocytosis, but [Ca2+]i elevations induced by photolysis of caged IP3 did trigger exocytosis, confirming that GnRH-stimulated gonadotropic hormone secretion is closely coupled to intracellular Ca2+ release. Agonist-induced oscillations of [Ca2+]i in secretory cells may be a mechanism to optimize the secretory output while avoiding the toxic effects of sustained elevation of [Ca2+]i.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tse, A -- Tse, F W -- Almers, W -- Hille, B -- New York, N.Y. -- Science. 1993 Apr 2;260(5104):82-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8385366" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium/*metabolism ; Calcium Channels/drug effects/physiology ; Cytoplasmic Granules/drug effects/physiology ; Electrophysiology ; Exocytosis/*drug effects ; Gonadotropin-Releasing Hormone/administration & dosage/*pharmacology ; Inositol 1,4,5-Trisphosphate/pharmacology ; Male ; Periodicity ; Photolysis ; Pituitary Gland/drug effects/*physiology/ultrastructure ; Rats ; Rats, Sprague-Dawley
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  • 88
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    Reduction in size of the myotonic dystrophy trinucleotide repeat mutation during transmission (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: Myotonic dystrophy (DM) is an autosomal-dominant disorder that affects 1 in 8000 individuals. Amplification of an unstable trinucleotide CTG repeat, located within the 3' untranslated region of a gene, correlates with a more severe DM phenotype. In three cases, the number of CTG repeats was reduced during the transmission of the DM allele; in one of these cases, the number was reduced to within the normal range and correlated at least with a delay in the onset of clinical signs of DM. Haplotype data of six polymorphic markers in the DM gene region indicate that, in this latter case, two stretches of the affected chromosome had been exchanged with that region of the wild-type chromosome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Hoy, K L -- Tsilfidis, C -- Mahadevan, M S -- Neville, C E -- Barcelo, J -- Hunter, A G -- Korneluk, R G -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):809-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of Ottawa, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8094260" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Age Factors ; Alleles ; Apolipoprotein C-II ; Apolipoproteins C/genetics ; Base Sequence ; *Chromosomes, Human, Pair 19 ; DNA/genetics/isolation & purification ; Female ; Genes, Dominant ; Haplotypes ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Myotonic Dystrophy/*genetics/physiopathology ; Oligodeoxyribonucleotides ; Pedigree ; Polymerase Chain Reaction ; *Polymorphism, Restriction Fragment Length ; *Repetitive Sequences, Nucleic Acid
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 89
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    CD40 ligand gene defects responsible for X-linked hyper-IgM syndrome (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-12
    Description: The ligand for CD40 (CD40L) is a membrane glycoprotein on activated T cells that induces B cell proliferation and immunoglobulin secretion. Abnormalities in the CD40L gene were associated with an X-linked immunodeficiency in humans [hyper-IgM (immunoglobulin M) syndrome]. This disease is characterized by elevated concentrations of serum IgM and decreased amounts of all other isotypes. CD40L complementary DNAs from three of four patients with this syndrome contained distinct point mutations. Recombinant expression of two of the mutant CD40L complementary DNAs resulted in proteins incapable of binding to CD40 and unable to induce proliferation or IgE secretion from normal B cells. Activated T cells from the four affected patients failed to express wild-type CD40L, although their B cells responded normally to wild-type CD40L. Thus, these CD40L defects lead to a T cell abnormality that results in the failure of patient B cells to undergo immunoglobulin class switching.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, R C -- Armitage, R J -- Conley, M E -- Rosenblatt, H -- Jenkins, N A -- Copeland, N G -- Bedell, M A -- Edelhoff, S -- Disteche, C M -- Simoneaux, D K -- A125129/PHS HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):990-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7679801" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*metabolism ; Antigens, CD40 ; Antigens, Differentiation, B-Lymphocyte/*metabolism ; Base Sequence ; CD40 Ligand ; DNA/chemistry/genetics ; Humans ; Immunoglobulin M/*blood ; Immunologic Deficiency Syndromes/*genetics/immunology ; Ligands ; Male ; Membrane Glycoproteins/*genetics ; Mice ; Molecular Sequence Data ; *Point Mutation ; Polymerase Chain Reaction ; T-Lymphocytes/*immunology ; Transfection ; *X Chromosome
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  • 90
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    Genetics and male sexual orientation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diamond, R -- New York, N.Y. -- Science. 1993 Sep 3;261(5126):1258-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8362240" target="_blank"〉PubMed〈/a〉
    Keywords: Civil Rights ; Ethics, Medical ; *Genes ; Genetic Testing ; *Homosexuality ; Humans ; Male
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 91
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    The skipping of constitutive exons in vivo induced by nonsense mutations (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-29
    Description: Nonsense mutations create a premature signal for the termination of translation of messenger RNA. Such mutations have been observed to cause a severe reduction in the amount of mutant allele transcript or to generate a peptide truncated at the carboxyl end. Analysis of fibrillin transcript from a patient with Marfan syndrome revealed the skipping of a constitutive exon containing a nonsense mutation. Similar results were observed for two nonsense mutations in the gene encoding ornithine delta-aminotransferase from patients with gyrate atrophy. All genomic DNA sequences flanking these exons that are known to influence RNA splicing were unaltered, which suggests that nonsense mutations can alter splice site selection in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dietz, H C -- Valle, D -- Francomano, C A -- Kendzior, R J Jr -- Pyeritz, R E -- Cutting, G R -- AR-41135/AR/NIAMS NIH HHS/ -- HG-00373/HG/NHGRI NIH HHS/ -- RR-00722/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Jan 29;259(5095):680-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430317" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cells, Cultured ; DNA/*genetics/isolation & purification ; *Exons ; Female ; Fibroblasts/physiology ; Humans ; Male ; Marfan Syndrome/*genetics ; Microfilament Proteins/*genetics ; Molecular Sequence Data ; *Mutation ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction/methods ; Reference Values
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  • 92
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    Involvement of platelet-endothelial cell adhesion molecule-1 in neutrophil recruitment in vivo (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-03
    Description: During inflammation, neutrophils migrate from the vascular lumen into extravascular sites. In vitro assays have suggested that platelet-endothelial cell adhesion molecule-1 [PECAM-1 (CD31)], a member of the immunoglobulin superfamily, is required for the transmigration of neutrophils across endothelial monolayers. Antibody to human PECAM-1, which cross-reacts with rat PECAM-1, was found to block not only in vivo accumulation of rat neutrophils into the peritoneal cavity and the alveolar compartment of the lung but also neutrophil accumulation in human skin grafts transplanted onto immunodeficient mice. On the basis of these findings in three different models of inflammation, it appears that PECAM-1 is required for neutrophil transmigration in vivo and may thus be a potential therapeutic target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vaporciyan, A A -- DeLisser, H M -- Yan, H C -- Mendiguren, I I -- Thom, S R -- Jones, M L -- Ward, P A -- Albelda, S M -- HL-31963/HL/NHLBI NIH HHS/ -- HL-430020-02/HL/NHLBI NIH HHS/ -- HL-46311/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 3;262(5139):1580-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Michigan Medical School, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8248808" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/pharmacology ; Antigens, CD31 ; Antigens, Differentiation, Myelomonocytic/immunology/*physiology ; Cell Adhesion Molecules/immunology/*physiology ; Cell Movement/physiology ; Chemotaxis, Leukocyte/physiology ; Endothelium/immunology ; Humans ; Immune Complex Diseases/immunology ; Membrane Glycoproteins/immunology/*physiology ; Mice ; Mice, SCID ; Neutrophils/*physiology ; Peritoneal Cavity/cytology ; Rats ; Skin Transplantation/immunology ; Transplantation, Heterologous/immunology
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  • 93
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    Sixth AIDS case traced to Florida dentist (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1993 May 14;260(5110):897.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493522" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*transmission ; *Dentists ; Female ; Florida ; Humans ; Male ; *Patients
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  • 94
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    Transsynaptic expression of a presynaptic glutamate receptor during hippocampal long-term potentiation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-15
    Description: Repetitive activation of excitatory synapses in the hippocampus produces a persistent enhancement of synaptic efficiency known as long-term potentiation (LTP). In anesthetized and in freely moving rats, the induction of LTP in the perforant path led to a transient increase in the amount of messenger RNA (mRNA) coding for a presynaptic glutamate receptor (GR33) in dentate granule cells. The amount of GR33 mRNA was increased for at least 5 hours after the induction of LTP but was indistinguishable from control values 1 day after induction. The N-methyl-D-aspartate receptor antagonist 2-aminophosphonovalerate prevented the induction of both LTP and the increase in GR33 mRNA. The amount of GR33 protein was increased in the mossy fiber terminal zone of dentate granule cells 5 hours after the induction of LTP. These results suggest that the induction of LTP in synapses at one stage in a neural network may lead to modification in synaptic function at the next stage in the network.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smirnova, T -- Laroche, S -- Errington, M L -- Hicks, A A -- Bliss, T V -- Mallet, J -- New York, N.Y. -- Science. 1993 Oct 15;262(5132):433-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de genetique moleculaire de la neurotransmission et des processus neurodegeneratifs, Centre National de la Recherche Scientifique (CNRS), Gif-sur-Yvette, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8105538" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Electric Stimulation ; Evoked Potentials ; Gene Expression ; Hippocampus/*metabolism/physiology ; In Situ Hybridization ; Male ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Glutamate/biosynthesis/*genetics ; Receptors, Presynaptic/biosynthesis/*genetics ; Synapses/*metabolism
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  • 95
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    Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-22
    Description: Genetic and metabolic studies have been done on a large kindred in which several males are affected by a syndrome of borderline mental retardation and abnormal behavior. The types of behavior that occurred include impulsive aggression, arson, attempted rape, and exhibitionism. Analysis of 24-hour urine samples indicated markedly disturbed monoamine metabolism. This syndrome was associated with a complete and selective deficiency of enzymatic activity of monoamine oxidase A (MAOA). In each of five affected males, a point mutation was identified in the eighth exon of the MAOA structural gene, which changes a glutamine to a termination codon. Thus, isolated complete MAOA deficiency in this family is associated with a recognizable behavioral phenotype that includes disturbed regulation of impulsive aggression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunner, H G -- Nelen, M -- Breakefield, X O -- Ropers, H H -- van Oost, B A -- NS 21921/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 22;262(5133):578-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, University Hospital Nijmegen, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211186" target="_blank"〉PubMed〈/a〉
    Keywords: *Aggression ; Cell Line ; Cells, Cultured ; Female ; *Genes ; Humans ; Intellectual Disability/enzymology/*genetics ; Male ; Monoamine Oxidase/deficiency/*genetics ; Pedigree ; Phenotype ; *Point Mutation ; Skin/enzymology ; Syndrome ; X Chromosome
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  • 96
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    Social structure of pilot whales revealed by analytical DNA profiling (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-04-30
    Description: Long-finned pilot whales swim in large, extremely cohesive social groups known as pods. Molecular typing revealed that pod members form a single extended family. Mature males neither disperse from nor mate within their natal pods, a situation unusual for mammals. Such behavior could be explained in terms of inclusive fitness benefits gained by adult males helping the large number of female relatives with which they swim.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amos, B -- Schlotterer, C -- Tautz, D -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):670-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Cambridge University, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480176" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; DNA, Satellite/*genetics ; Female ; Genotype ; Male ; Molecular Sequence Data ; Oligodeoxyribonucleotides/genetics ; Repetitive Sequences, Nucleic Acid ; Sexual Behavior, Animal ; *Social Behavior ; Whales/genetics/*physiology
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  • 97
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    Modulation of cocaine self-administration in the rat through D-3 dopamine receptors (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-06-18
    Description: The reinforcing properties of cocaine are probably mediated by the mesocorticolimbic dopamine pathways in the central nervous system, but not all of the dopamine receptor subtypes involved in cocaine's reinforcing actions have been clearly identified. Recently, the D-3 receptor has been cloned, and its distribution in the brain has been found to be relatively restricted to limbic projections of the midbrain dopamine system. The D-3-selective compounds 7-hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OHDPAT) and quinpirole potently decreased cocaine self-administration in the rat at doses that were not by themselves reinforcing. Moreover, three dopamine receptor agonists had affinities for binding to the D-3 receptor that correlated highly with their relative potencies in decreasing cocaine self-administration. The D-3 receptor may be involved in the reinforcing effects of cocaine and may be a useful target for the development of new pharmacotherapies for cocaine abuse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caine, S B -- Koob, G F -- NIDA DA04398/DA/NIDA NIH HHS/ -- NIDA DA05478/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1814-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuropharmacology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8099761" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apomorphine/pharmacology ; Cocaine/*administration & dosage ; Dopamine Agents/*pharmacology ; Dose-Response Relationship, Drug ; Ergolines/pharmacology ; Male ; Quinpirole ; Rats ; Rats, Wistar ; Receptors, Dopamine/*metabolism ; *Receptors, Dopamine D2 ; Receptors, Dopamine D3 ; Reinforcement (Psychology) ; Self Administration ; Tetrahydronaphthalenes/pharmacology
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  • 98
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    Functional magnetic resonance imaging of motor cortex: hemispheric asymmetry and handedness (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-30
    Description: A hemispheric asymmetry in the functional activation of the human motor cortex during contralateral (C) and ipsilateral (I) finger movements, especially in right-handed subjects, was documented with nuclear magnetic resonance imaging at high field strength (4 tesla). Whereas the right motor cortex was activated mostly during contralateral finger movements in both right-handed (C/I mean area of activation = 36.8) and left-handed (C/I = 29.9) subjects, the left motor cortex was activated substantially during ipsilateral movements in left-handed subjects (C/I = 5.4) and even more so in right-handed subjects (C/I = 1.3).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, S G -- Ashe, J -- Hendrich, K -- Ellermann, J M -- Merkle, H -- Ugurbil, K -- Georgopoulos, A P -- HL32427/HL/NHLBI NIH HHS/ -- HL33600/HL/NHLBI NIH HHS/ -- RR08079/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 30;261(5121):615-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Magnetic Resonance Research (CMRR), University of Minnesota Medical School, Minneapolis 55455.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342027" target="_blank"〉PubMed〈/a〉
    Keywords: *Brain Mapping ; Female ; *Functional Laterality ; Humans ; *Magnetic Resonance Imaging ; Male ; Motor Cortex/anatomy & histology/*physiology
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  • 99
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    A linkage between DNA markers on the X chromosome and male sexual orientation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-16
    Description: The role of genetics in male sexual orientation was investigated by pedigree and linkage analyses on 114 families of homosexual men. Increased rates of same-sex orientation were found in the maternal uncles and male cousins of these subjects, but not in their fathers or paternal relatives, suggesting the possibility of sex-linked transmission in a portion of the population. DNA linkage analysis of a selected group of 40 families in which there were two gay brothers and no indication of nonmaternal transmission revealed a correlation between homosexual orientation and the inheritance of polymorphic markers on the X chromosome in approximately 64 percent of the sib-pairs tested. The linkage to markers on Xq28, the subtelomeric region of the long arm of the sex chromosome, had a multipoint lod score of 4.0 (P = 10(-5), indicating a statistical confidence level of more than 99 percent that at least one subtype of male sexual orientation is genetically influenced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hamer, D H -- Hu, S -- Magnuson, V L -- Hu, N -- Pattatucci, A M -- New York, N.Y. -- Science. 1993 Jul 16;261(5119):321-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332896" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; *Genes ; *Genetic Linkage ; Genetic Markers ; Genotype ; *Homosexuality ; Humans ; Male ; Pedigree ; Phenotype ; *X Chromosome
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  • 100
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    Thinking about brain cell assemblies (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eichenbaum, H -- New York, N.Y. -- Science. 1993 Aug 20;261(5124):993-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Behavioral Neuroscience, State University of New York, Stony Brook 11794.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8351525" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Cerebral Cortex/physiology ; Hippocampus/*physiology ; *Memory ; Neurons/*physiology ; *Perception ; Rats
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