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  • 11
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-06-16
    Description: Food deprivation and weight loss inhibit ovulation and estrous behavior in Syrian hamsters. In the present experiments, lean hamsters were more susceptible to starvation-induced anestrus than fat hamsters. However, anestrus was not caused by changes in any dimension of body size per se, but instead by the availability of metabolic fuels. Simultaneous pharmacological blockade of both fatty acid oxidation and glycolysis inhibited reproduction, but, as long as one of these metabolic pathways could be used, estrous cycles continued. Thus, reproduction in female Syrian hamsters is sensitive to the general availability of oxidizable metabolic fuels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schneider, J E -- Wade, G N -- AM 32976-06/AM/NIADDK NIH HHS/ -- MH 00321-09/MH/NIMH NIH HHS/ -- NS 10873-17/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1326-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Massachusetts, Amherst 01003.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2734610" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimetabolites/pharmacology ; Body Weight ; Cricetinae ; Deoxyglucose/pharmacology ; Epoxy Compounds/pharmacology ; Estrus/drug effects/*physiology ; Female ; Food Deprivation/*physiology ; Mesocricetus ; Periodicity ; Propionates/pharmacology
    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
    Publication Date: 1988-04-15
    Description: Immunization with radiation-attenuated malaria sporozoites induces potent cellular immune responses, but the target antigens are unknown and have not previously been elicited by subunit vaccines prepared from the circumsporozoite (CS) protein. A method is described here for inducing protective cell-mediated immunity to sporozoites by immunization with attenuated Salmonella typhimurium transformed with the Plasmodium berghei CS gene. These transformants constitutively express CS antigens and, when used to immunize mice orally, colonize the liver, induce antigen-specific cell-mediated immunity, and protect mice against sporozoite challenge in the absence of antisporozoite antibodies. These data indicate that the CS protein contains T cell epitopes capable of inducing protective cell-mediated immunity, and emphasize the importance of proper antigen presentation in generating this response. Analogous, orally administered vaccines against human malaria might be feasible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sadoff, J C -- Ballou, W R -- Baron, L S -- Majarian, W R -- Brey, R N -- Hockmeyer, W T -- Young, J F -- Cryz, S J -- Ou, J -- Lowell, G H -- New York, N.Y. -- Science. 1988 Apr 15;240(4850):336-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacterial Diseases, Walter Reed Army Institute of Research, Washington, DC 20307-5100.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3281260" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/*immunology ; Bacterial Vaccines/*immunology ; Female ; Liver/microbiology ; Malaria/*immunology/prevention & control ; Mice ; Mice, Inbred BALB C ; Plasmids ; Plasmodium berghei/*immunology ; *Protozoan Proteins ; Salmonella typhimurium/genetics/*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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  • 13
    Publication Date: 1988-03-11
    Description: The alterations in morphology and function of the ovarian follicle as it matures, ovulates, and becomes a corpus luteum are dramatic. A variety of steroid and polypeptide hormones influence these processes, and the ovary in turn produces specific hormonal signals for endocrine regulation. One such signal is inhibin, a heterodimeric protein that suppresses the secretion of follicle-stimulating hormone from pituitary gonadotrophs. Rat inhibin complementary DNA probes have been used to examine the levels and distribution of inhibin alpha-and beta A-subunit messenger RNAs in the ovaries of cycling animals. Striking, dynamic changes have been found in inhibin messenger RNA accumulation during the developmental maturation of the ovarian follicle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woodruff, T K -- D'Agostino, J -- Schwartz, N B -- Mayo, K E -- HD07504/HD/NICHD NIH HHS/ -- HD21921/HD/NICHD NIH HHS/ -- P01 HD021921/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1296-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3125611" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Estrus ; Female ; Follicle Stimulating Hormone/blood ; Inhibins/*genetics ; Luteinizing Hormone/blood ; Macromolecular Substances ; Nucleic Acid Hybridization ; Ovarian Follicle/*physiology ; Ovary/physiology ; RNA, Messenger/*genetics/metabolism ; Rats
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  • 14
    Publication Date: 1986-05-02
    Description: The development of simultaneous resistance to multiple structurally unrelated drugs is a major impediment to cancer chemotherapy. Multidrug resistance in human KB carcinoma cells selected in colchicine, vinblastine, or Adriamycin is associated with amplification of specific DNA sequences (the multidrug resistance locus, mdr1). During colchicine selection resistance is initially accompanied by elevated expression of a 4.5-kilobase mdr1 messenger RNA (mRNA) without amplification of the corresponding genomic sequences. During selection for increased levels of resistance, expression of this mRNA is increased simultaneously with amplification of mdr1 DNA. Increased expression and amplification of mdr1 sequences were also found in multidrug-resistant sublines of human leukemia and ovarian carcinoma cells. These results suggest that increased expression of mdr1 mRNA is a common mechanism for multidrug resistance in human cells. Activation of the mdr1 gene by mutations or epigenetic changes may precede its amplification during the development of resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, D W -- Fojo, A -- Chin, J E -- Roninson, I B -- Richert, N -- Pastan, I -- Gottesman, M M -- New York, N.Y. -- Science. 1986 May 2;232(4750):643-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3457471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Colchicine/pharmacology ; Cricetinae ; Cricetulus ; DNA, Neoplasm/genetics ; Doxorubicin/pharmacology ; *Drug Resistance ; Female ; *Gene Amplification ; Humans ; Leukemia, Lymphoid/drug therapy ; Neoplasms/*drug therapy/genetics ; Nucleic Acid Hybridization ; Ovarian Neoplasms/drug therapy ; RNA, Messenger/genetics ; Vinblastine/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
    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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-08-12
    Description: Receptors for N-methyl-D-aspartate (NMDA) are involved in many plastic and pathological processes in the brain. Glycine has been reported to potentiate NMDA responses in neurons and in Xenopus oocytes injected with rat brain messenger RNA. Glycine is now shown to be absolutely required for activation of NMDA receptors in oocytes. In voltage-clamped oocytes, neither perfusion nor rapid pressure application of NMDA onto messenger RNA-injected oocytes caused a distinct ionic current without added glycine. When glycine was added, however, NMDA evoked large inward currents. The concentration of glycine required to produce a half-maximal response was 670 nanomolar, and the glycine dose-response curve extrapolated to zero in the absence of glycine. Several analogs of glycine could substitute for glycine, among which D-serine and D-alanine were the most effective. The observation that D-amino acids are effective will be important in developing drugs targeted at the glycine site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kleckner, N W -- Dingledine, R -- NS17771/NS/NINDS NIH HHS/ -- NS22249/NS/NINDS NIH HHS/ -- NS23804/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 12;241(4867):835-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of North Carolina, Chapel Hill 27599-7365.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2841759" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/pharmacology ; Animals ; Brain/metabolism ; Female ; Glycine/*analogs & derivatives/*pharmacology ; Kinetics ; Oocytes/drug effects/*metabolism ; RNA, Messenger/genetics ; Rats ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/drug effects/genetics/*metabolism ; Xenopus
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  • 17
    Publication Date: 1988-12-16
    Description: Site-directed mutagenesis and expression in Xenopus oocytes were used to study acetylcholine receptors in which serine residues (i) were replaced by alanines (alpha, delta subunits) or (ii) replaced a phenylalanine (beta subunit) at a postulated polar site within the M2 transmembrane helix. As the number of serines decreased, there were decreases in the residence time and consequently the equilibrium binding affinity of QX-222, a quaternary ammonium anesthetic derivative thought to bind within the open channel. Receptors with three serine-to-alanine mutations also displayed a selective decrease in outward single-channel currents. Both the direction of this rectification and the voltage dependence of QX-222 blockade suggest that the residues mutated are within the aqueous pore of the receptor and near its cytoplasmic (inner) surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leonard, R J -- Labarca, C G -- Charnet, P -- Davidson, N -- Lester, H A -- NS-11756/NS/NINDS NIH HHS/ -- NS-8083/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 16;242(4885):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2462281" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/*physiology ; Cloning, Molecular ; Electric Conductivity ; Female ; Ion Channels/*physiology ; Kinetics ; Membrane Potentials ; Mutation ; Oocytes/physiology ; RNA, Messenger/genetics ; Receptors, Nicotinic/genetics/*physiology ; Transcription, Genetic ; Xenopus
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  • 18
    Publication Date: 1985-02-01
    Description: Eleven mangabey monkeys inoculated with Mycobacterium leprae developed lepromatous-type leprosy. Nine of the mangabeys were inoculated with M. leprae isolated from a mangabey with naturally acquired lepromatous leprosy. Immune function was depressed in some of these animals after dissemination of the disease. Two mangabeys developed lepromatous leprosy after inoculation with human M. leprae passaged in an armadillo. Three rhesus and three African green monkeys inoculated with mangabey-derived M. leprae also developed lepromatous leprosy. Mangabeys may be the first reported nonhuman primate model for the study of leprosy. Rhesus and African green monkeys may also prove to be reproducibly susceptible to the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolf, R H -- Gormus, B J -- Martin, L N -- Baskin, G B -- Walsh, G P -- Meyers, W M -- Binford, C H -- 5R-22-AI-19302/AI/NIAID NIH HHS/ -- RR-00164/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1985 Feb 1;227(4686):529-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3917577" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Bacterial/analysis ; Cercopithecidae ; Cercopithecus aethiops ; *Disease Models, Animal ; Disease Susceptibility ; Female ; *Haplorhini ; *Leprosy/immunology/pathology/transmission ; Lymphocyte Activation ; Macaca mulatta ; Male ; Mycobacterium leprae/immunology ; Saimiri ; Species Specificity
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  • 19
    Publication Date: 1986-08-15
    Description: Transplantation of normal, immature, fetal hematopoietic cells into a preimmune fetal recipient with a congenital hemoglobinopathy may allow partial reconstitution of normal hemoglobin production without the complications associated with postnatal bone marrow transplantation (immunosuppression and the occurrence of graft versus host disease). In order to test this hypothesis the naturally occurring polymorphism at the beta-hemoglobin locus of the sheep was used as a marker for engraftment and hematopoietic chimerism. Intraperitoneal injection of allogeneic fetal stem cells into normal fetal lambs resulted in hematopoietic chimerism in three of four surviving recipients. This chimerism has been sustained for 6 months after birth and 9 months after engraftment, without evidence of graft versus host disease, and without the use of immunosuppressive therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flake, A W -- Harrison, M R -- Adzick, N S -- Zanjani, E D -- AM-24027/AM/NIADDK NIH HHS/ -- AM-29890/AM/NIADDK NIH HHS/ -- AM-30914/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 15;233(4765):776-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2874611" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chimera ; Female ; Fetus ; Graft vs Host Disease ; *Hematopoietic Stem Cell Transplantation ; Hemoglobin A/*analysis ; Hemoglobins/*analysis ; Pregnancy ; Sheep ; Transplantation, Homologous
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  • 20
    Publication Date: 1986-12-12
    Description: The hypogonadal (hpg) mouse lacks a complete gonadotropin-releasing hormone (GnRH) gene and consequently cannot reproduce. Introduction of an intact GnRH gene into the genome of these mutant mice resulted in complete reversal of the hypogonadal phenotype. Transgenic hpg/hpg homozygotes of both sexes were capable of mating and producing offspring. Pituitary and serum concentrations of luteinizing hormone, follicle-stimulating hormone, and prolactin were restored to those of normal animals. Immunocytochemistry and in situ hybridization showed that GnRH expression was restored in the appropriate hypothalamic neurons of the transgenic hpg animals, an indication of neural-specific expression of the introduced gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mason, A J -- Pitts, S L -- Nikolics, K -- Szonyi, E -- Wilcox, J N -- Seeburg, P H -- Stewart, T A -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1372-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3097822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Follicle Stimulating Hormone/blood ; Gene Expression Regulation ; *Genetic Engineering ; Gonadotropin-Releasing Hormone/genetics ; Histocytochemistry ; Hypogonadism/*genetics ; Hypothalamus/analysis/cytology ; Infertility/genetics/*therapy ; Luteinizing Hormone/blood ; Male ; Mice ; Mutation ; Neurons/analysis ; Phenotype ; Prolactin/blood ; Tissue Distribution
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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