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  • 1
    Publication Date: 1987-02-13
    Description: A highly T-lymphotropic virus was isolated from cats in a cattery in which all the animals were seronegative for feline leukemia virus. A number of cats in one pen had died and several had an immunodeficiency-like syndrome. Only 1 of 18 normal cats in the cattery showed serologic evidence of infection with this new virus, whereas 10 of 25 cats with signs of ill health were seropositive for the virus. Tentatively designated feline T-lymphotropic lentivirus, this new feline retrovirus appears to be antigenically distinct from human immunodeficiency virus. There is no evidence for cat-to-human transmission of the agent. Kittens experimentally infected by way of blood or plasma from naturally infected animals developed generalized lymphadenopathy several weeks later, became transiently febrile and leukopenic, and continued to show a generalized lymphadenopathy 5 months after infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pedersen, N C -- Ho, E W -- Brown, M L -- Yamamoto, J K -- CA-39016-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 13;235(4790):790-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3643650" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Viral/analysis ; Cat Diseases/*microbiology ; Cats/*microbiology ; Female ; HIV/immunology ; Immunologic Deficiency Syndromes/microbiology/*veterinary ; Lymphocytes/ultrastructure ; Male ; Microscopy, Electron ; Retroviridae/immunology/*isolation & purification/ultrastructure ; Species Specificity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1987-09-25
    Description: The gene responsible for Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) maps to the X chromosome short arm, band Xp21. In a few females with DMD or BMD, the Xp21 region is disrupted by an X-autosome translocation. Accumulating evidence suggests that the exchange has physically disrupted the DMD/BMD locus to cause the disease. One affected female with a t(X;21)(p21;p12) translocation was studied in detail. The exchange points from both translocation chromosomes were cloned, restriction-mapped, and sequenced. The translocation is reciprocal, but not conservative. A small amount of DNA is missing from the translocated chromosomes; 71 to 72 base pairs from the X chromosome and 16 to 23 base pairs from the 28S ribosomal gene on chromosome 21.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bodrug, S E -- Ray, P N -- Gonzalez, I L -- Schmickel, R D -- Sylvester, J E -- Worton, R G -- New York, N.Y. -- Science. 1987 Sep 25;237(4822):1620-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629260" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; *Chromosomes, Human, Pair 21 ; Cloning, Molecular ; DNA, Ribosomal/genetics ; Female ; Humans ; Muscular Dystrophies/*genetics ; Pedigree ; RNA, Ribosomal/genetics ; *Translocation, Genetic ; *X Chromosome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1987-09-04
    Description: The steroid hormones corticosterone and testosterone are supplied to the central nervous system by endocrine glands, the adrenals and gonads. In contrast, the 3 beta-hydroxy-delta 5-derivatives of cholesterol, pregnenolone and dehydroepiandrosterone, accumulate in the rat brain through mechanisms independent of peripheral sources. Immunohistochemical studies have been performed with specific antibodies to bovine adrenal cytochrome P-450scc, which is involved in cholesterol side-chain cleavage and pregnenolone formation. The enzyme was localized in the white matter throughout the brain. Scarce clusters of cell bodies were also stained in the entorhinal and cingulate cortex and in the olfactory bulb. These observations strongly support the existence of "neurosteroids," which have been posited on the basis of biochemical, physiological, and behavioral studies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Le Goascogne, C -- Robel, P -- Gouezou, M -- Sananes, N -- Baulieu, E E -- Waterman, M -- New York, N.Y. -- Science. 1987 Sep 4;237(4819):1212-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3306919" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/metabolism ; Animals ; Brain/cytology/*metabolism ; Cholesterol Side-Chain Cleavage Enzyme/*metabolism ; Female ; Histocytochemistry ; Hormones/*biosynthesis ; Immunoenzyme Techniques ; Oxidoreductases/*metabolism ; Rats ; Steroids/*biosynthesis ; Tissue Distribution
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 1987-03-06
    Description: Under the influence of estrogen, uterine smooth muscle becomes highly excitable, generating spontaneous and prolonged bursts of action potentials. In a study of the mechanisms by which this transition in excitability occurs, polyadenylated RNA from the uteri of estrogen-treated rats was injected into Xenopus oocytes. The injected oocytes expressed a novel voltage-dependent potassium current. This current was not observed in oocytes injected with RNA from several other excitable tissues, including rat brain and uterine smooth muscle from ovariectomized rats not treated with estrogen. The activation of this current on depolarization was exceptionally slow, particularly for depolarizations from relatively negative membrane potentials. Such a slowly activating channel may play an important role in the slow, repetitive bursts of action potentials in the myometrium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyle, M B -- Azhderian, E M -- MacLusky, N J -- Naftolin, F -- Kaczmarek, L K -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1221-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2434999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/pharmacology ; Egtazic Acid/pharmacology ; Female ; Injections ; Ion Channels/*metabolism ; Oocytes/*metabolism ; Potassium/*metabolism ; RNA/*pharmacology ; Rats ; Rats, Inbred Strains ; Time Factors ; Uterus/*metabolism ; Xenopus
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 1987-09-04
    Description: Many spontaneous mutations are caused by the insertion or excision of DNA elements. Since most mutations are deleterious, evolution should favor a mechanism for genetically controlling the rate of movement of transposable elements in most, if not all, organisms. In Drosophila melanogaster a syndrome of correlated genetic changes, including mutation, chromosome breakage, and sterility, is observed in the hybrid progeny of crosses between different strains. This syndrome, which is termed hybrid dysgenesis, results from the movement of P-DNA elements. What is not clear is whether the movement of other types of transposable elements is under the same coordinated control. In this study the ability of hybrid dysgenesis to increase the rate of excision of 12 DNA elements at 16 mutant alleles and to induce insertion-bearing mutations to change to other mutant states was tested. The data show that hybrid dysgenesis caused by P-element transpositions does not act as a general stimulus for the movement of other Drosophila transposable elements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woodruff, R C -- Blount, J L -- Thompson, J N Jr -- K04-ES-00087/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1987 Sep 4;237(4819):1206-18.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2820057" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crosses, Genetic ; *DNA Transposable Elements ; Drosophila melanogaster/*genetics ; Female ; Gonadal Dysgenesis ; Hybridization, Genetic ; Male ; Mutation ; Probability
    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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