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  • Animals  (32)
  • American Association for the Advancement of Science (AAAS)  (32)
  • American Institute of Physics
  • 1995-1999  (12)
  • 1990-1994  (20)
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  • American Association for the Advancement of Science (AAAS)  (32)
  • American Institute of Physics
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  • 1
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    Mutagenesis and mapping of a mouse gene, Clock, essential for circadian behavior (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-29
    Description: In a search for genes that regulate circadian rhythms in mammals, the progeny of mice treated with N-ethyl-N-nitrosourea (ENU) were screened for circadian clock mutations. A semidominant mutation, Clock, that lengthens circadian period and abolishes persistence of rhythmicity was identified. Clock segregated as a single gene that mapped to the midportion of mouse chromosome 5, a region syntenic to human chromosome 4. The power of ENU mutagenesis combined with the ability to clone murine genes by map position provides a generally applicable approach to study complex behavior in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839659/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839659/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vitaterna, M H -- King, D P -- Chang, A M -- Kornhauser, J M -- Lowrey, P L -- McDonald, J D -- Dove, W F -- Pinto, L H -- Turek, F W -- Takahashi, J S -- P30-CA07175/CA/NCI NIH HHS/ -- R01-DK40493/DK/NIDDK NIH HHS/ -- T32 NS071040/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- etc. -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):719-25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171325" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Chromosomes, Human, Pair 4 ; Circadian Rhythm/*genetics ; Ethylnitrosourea ; Female ; *Genes ; Genotype ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; *Mutagenesis ; Phenotype
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Impaired B cell development and proliferation in absence of phosphoinositide 3-kinase p85alpha (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: Phosphoinositide 3-kinase (PI3K) activation has been implicated in many cellular responses, including fibroblast growth, transformation, survival, and chemotaxis. Although PI3K is activated by several agents that stimulate T and B cells, the role of PI3K in lymphocyte function is not clear. The mouse gene encoding the PI3K adapter subunit p85alpha and its splice variants p55alpha and p50alpha was disrupted. Most p85alpha-p55alpha-p50alpha-/- mice die within days after birth. Lymphocyte development and function was studied with the use of the RAG2-deficient blastocyst complementation system. Chimeric mice had reduced numbers of peripheral mature B cells and decreased serum immunoglobulin. The B cells that developed had diminished proliferative responses to antibody to immunoglobulin M, antibody to CD40, and lipopolysaccharide stimulation and decreased survival after incubation with interleukin-4. In contrast, T cell development and proliferation was normal. This phenotype is similar to defects observed in mice lacking the tyrosine kinase Btk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fruman, D A -- Snapper, S B -- Yballe, C M -- Davidson, L -- Yu, J Y -- Alt, F W -- Cantley, L C -- R01 GM041890/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):393-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. dfruman@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD45/analysis ; Apoptosis ; B-Lymphocytes/cytology/enzymology/*immunology ; Catalytic Domain ; Cell Cycle ; Chimera ; Chromones/pharmacology ; Enzyme Inhibitors/pharmacology ; Female ; Gene Targeting ; Immunoglobulins/*blood ; *Lymphocyte Activation ; Lymphocyte Count ; Male ; Mice ; Mice, Inbred C57BL ; Morpholines/pharmacology ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors/genetics/*metabolism ; Protein-Tyrosine Kinases/genetics/metabolism ; Spleen/immunology ; T-Lymphocytes/cytology/enzymology/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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  • 3
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    Cell-adhesive motif in region II of malarial circumsporozoite protein (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-28
    Description: The segment of the malarial circumsporozoite (CS) protein designated Region II is highly conserved among different malarial species. A similar sequence is also present in several other proteins, including thrombospondin, properdin, and a blood-stage antigen of Plasmodium falciparum. By means of peptides synthesized from sequences of the Plasmodium vivax CS protein in the vicinity of Region II, it was found that two overlapping 18- to 20-amino acid peptides promoted the adhesion of a variety of human hematopoietic cell lines. The amino acid sequence valine-threonine-cysteineglycine (VTCG), contained within this common motif, was shown to be the critical sequence for the observed cell-adhesive properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rich, K A -- George, F W 4th -- Law, J L -- Martin, W J -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Southern California School of Medicine, Los Angeles 90033.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2120774" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Protozoan/*genetics ; *Cell Adhesion ; Cell Line ; Fluorescein-5-isothiocyanate ; Fluoresceins ; Fluorescent Dyes ; Humans ; Molecular Sequence Data ; Peptides/chemical synthesis ; Plasmodium falciparum/*genetics ; Plasmodium vivax/*genetics ; Protozoan Proteins/*genetics ; Thiocyanates
    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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    Strontianite in coral skeletal aragonite (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-07
    Description: An x-ray spectroscopic study of scleractinian coral skeletons indicated that, although some strontium substitutes for calcium in the aragonite structure, at concentrations of about 7500 parts per million, as much as 40 percent of the strontium resides in strontianite (SrCO3). A doublet peak in the Fourier transform of the extended x-ray absorption fine structure of the coral corresponded to six metal and 13 oxygen neighbors surrounding strontium at about 4.05 angstroms in strontium-substituted aragonite and at about 4.21 angstroms in strontianite. Thus, the mechanism of the temperature-sensitive partitioning of strontium between seawater and coral skeleton used for paleothermometry is unexpectedly complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greegor, R B -- Pingitore, N E Jr -- Lytle, F W -- New York, N.Y. -- Science. 1997 Mar 7;275(5305):1452-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Boeing Company, Seattle, WA 98124, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072808" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/analysis ; Calcium Carbonate/*analysis ; Carbonates/*analysis ; Cnidaria/*chemistry ; Fourier Analysis ; Spectrum Analysis ; Strontium/*analysis ; Temperature
    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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    Thymocyte development in the absence of pre-T cell receptor extracellular immunoglobulin domains (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-23
    Description: Immature thymocytes express a pre-T cell receptor (pre-TCR) composed of the TCRbeta chain paired with pre-Talpha. Signals from this receptor are essential for passage of thymocytes through a key developmental checkpoint in the thymus. These signals were efficiently delivered in vivo by a truncated form of the murine pre-TCR that lacked all of its extracellular immunoglobulin domains. De novo expression of the truncated pre-TCR or an intact alphabetaTCR was sufficient to activate characteristic TCR signaling pathways in a T cell line. These findings support the view that recognition of an extracellular ligand is not required for pre-TCR function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Irving, B A -- Alt, F W -- Killeen, N -- New York, N.Y. -- Science. 1998 May 8;280(5365):905-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California, San Francisco, CA 94143-0414, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9572735" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/analysis ; Antigens, CD3/analysis/genetics ; DNA-Binding Proteins/genetics/metabolism ; Dimerization ; Gene Rearrangement, T-Lymphocyte ; Humans ; Immunoglobulins/chemistry ; Immunophenotyping ; Jurkat Cells ; Ligands ; Membrane Glycoproteins/chemistry/genetics/*physiology ; Mice ; Mice, Inbred Strains ; Mice, Transgenic ; NFATC Transcription Factors ; *Nuclear Proteins ; Receptors, Antigen, T-Cell, alpha-beta/chemistry/genetics/*physiology ; Signal Transduction ; T-Lymphocytes/cytology/*immunology/metabolism ; Transcription Factors/genetics/metabolism ; Transfection
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  • 6
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    Disappearance of the lymphoid system in Bcl-2 homozygous mutant chimeric mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-17
    Description: The bcl-2 proto-oncogene can prevent the death of many cell types. Mice were generated that were chimeric for the homozygous inactivation of bcl-2. Lymphocytes without Bcl-2 differentiated into phenotypically mature cells. However, in vitro, the mature T cells that lacked Bcl-2 had shorter life-spans and increased sensitivity to glucocorticoids and gamma-irradiation. In contrast, stimulation of CD3 inhibited the death of these cells. T and B cells with no Bcl-2 disappeared from the bone marrow, thymus, and periphery by 4 weeks of age. Thus, Bcl-2 was dispensable for lymphocyte maturation, but was required for a stable immune system after birth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakayama, K -- Negishi, I -- Kuida, K -- Shinkai, Y -- Louie, M C -- Fields, L E -- Lucas, P J -- Stewart, V -- Alt, F W -- AI 15322/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 17;261(5128):1584-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8372353" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3/immunology ; Apoptosis ; B-Lymphocytes/cytology/*immunology ; Base Sequence ; Bone Marrow/immunology ; Bone Marrow Cells ; Cell Line ; Chimera ; Homozygote ; Humans ; Lymphoid Tissue/cytology/immunology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins c-bcl-2 ; Proto-Oncogenes ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/cytology/*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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  • 7
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    Attomole protein characterization by capillary electrophoresis-mass spectrometry (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-30
    Description: Electrospray ionization with an ultralow flow rate (〈/=4 nanoliters per minute) was used to directly couple capillary electrophoresis with tandem mass spectrometry for the analysis and identification of biomolecules in mixtures. A Fourier transform mass spectrometer provided full spectra (〉30 kilodaltons) at a resolving power of approximately 60,000 for injections of 0.7 x 10(-18) to 3 x 10(-18) mole of 8- to 29-kilodalton proteins with errors of 〈1 dalton in molecular mass. Using a crude isolate from human blood, a value of 28,780.6 daltons (calculated, 28,780.4 daltons) was measured for carbonic anhydrase, representing 1 percent by weight of the protein in a single red blood cell. Dissociation of molecular ions from 9 x 10(-18) mole of carbonic anhydrase gave nine sequence-specific fragment ions, more data than required for unique retrieval of this enzyme from the protein database.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Valaskovic, G A -- Kelleher, N L -- McLafferty, F W -- 08-T2GM07273/GM/NIGMS NIH HHS/ -- GM16609/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 30;273(5279):1199-202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Baker Laboratory, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8703047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbonic Anhydrases/*analysis/chemistry ; Cattle ; Cytochrome c Group/analysis/chemistry ; Electrophoresis, Capillary/*methods ; Horses ; Humans ; Mass Spectrometry/*methods ; Molecular Weight ; Proteins/*analysis/chemistry ; Sensitivity and Specificity ; Spectroscopy, Fourier Transform Infrared ; Ubiquitins/analysis/chemistry
    Print ISSN: 0036-8075
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  • 8
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    Synaptic efficacy enhanced by glial cells in vitro (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-12
    Description: In the developing nervous system, glial cells guide axons to their target areas, but it is unknown whether they help neurons to establish functional synaptic connections. The role of glial cells in synapse formation and function was studied in cultures of purified neurons from the rat central nervous system. In glia-free cultures, retinal ganglion cells formed synapses with normal ultrastructure but displayed little spontaneous synaptic activity and high failure rates in evoked synaptic transmission. In cocultures with neuroglia, the frequency and amplitude of spontaneous postsynaptic currents were potentiated by 70-fold and 5-fold, respectively, and fewer transmission failures occurred. Glial cells increased the action potential-independent quantal release by 12-fold without affecting neuronal survival. Thus, developing neurons in culture form inefficient synapses that require glial signals to become fully functional.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfrieger, F W -- Barres, B A -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1684-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Stanford University, School of Medicine, Sherman Fairchild Science Building, 299 Campus Drive, Stanford, CA 94305-5125, USA. fpfrieg@mdc-berlin.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9287225" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Astrocytes/physiology ; Cell Survival ; Cells, Cultured ; Coculture Techniques ; Microglia/physiology ; Neuroglia/*physiology ; Oligodendroglia/physiology ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells/cytology/*physiology/ultrastructure ; Synapses/*physiology/ultrastructure ; *Synaptic Transmission
    Print ISSN: 0036-8075
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  • 9
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    Blocked Ras activation in anergic CD4+ T cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: T cell anergy is a state of functional unresponsiveness characterized by the inability to produce interleukin-2 (IL-2) upon T cell receptor stimulation. The mitogen-activated protein kinases ERK-1 and ERK-2 and the guanosine triphosphate-binding protein p21ras were found to remain unactivated upon stimulation of anergic murine T helper cell 1 clones. The inability to activate the Ras pathway did not result from a defect in association among Shc, Grb-2, and murine Son of Sevenless, nor from a defect in their tyrosine phosphorylation. This block in Ras activation may lead to defective transactivation at activator protein 1 sites in anergic cells and may enable T cells to shut down IL-2 production selectively during anergy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fields, P E -- Gajewski, T F -- Fitch, F W -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1276-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ben May Institute, Department of Pathology, University of Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638108" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD4/immunology ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; *Clonal Anergy ; Clone Cells ; GRB2 Adaptor Protein ; Guanine Nucleotide Exchange Factors ; Guanosine Triphosphate/metabolism ; Interleukin-2/biosynthesis ; Ionomycin/pharmacology ; Lymphocyte Activation ; Mice ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Protein-Tyrosine Kinases/metabolism ; Proteins/metabolism ; Proto-Oncogene Proteins p21(ras)/*metabolism ; Receptors, Antigen, T-Cell/immunology ; *Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Th1 Cells/*immunology/metabolism ; ras Guanine Nucleotide Exchange Factors
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  • 10
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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