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  • Male  (403)
  • American Association for the Advancement of Science (AAAS)  (403)
  • 1990-1994  (403)
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  • American Association for the Advancement of Science (AAAS)  (403)
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  • 1
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    Effects of cerebral ischemia in mice deficient in neuronal nitric oxide synthase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: The proposal that nitric oxide (NO) or its reactant products mediate toxicity in brain remains controversial in part because of the use of nonselective agents that block NO formation in neuronal, glial, and vascular compartments. In mutant mice deficient in neuronal NO synthase (NOS) activity, infarct volumes decreased significantly 24 and 72 hours after middle cerebral artery occlusion, and the neurological deficits were less than those in normal mice. This result could not be accounted for by differences in blood flow or vascular anatomy. However, infarct size in the mutant became larger after endothelial NOS inhibition by nitro-L-arginine administration. Hence, neuronal NO production appears to exacerbate acute ischemic injury, whereas vascular NO protects after middle cerebral artery occlusion. The data emphasize the importance of developing selective inhibitors of the neuronal isoform.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Z -- Huang, P L -- Panahian, N -- Dalkara, T -- Fishman, M C -- Moskowitz, M A -- NS10828/NS/NINDS NIH HHS/ -- NS2636/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1883-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stroke Research Laboratory, Massachusetts General Hospital, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522345" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/antagonists & inhibitors/deficiency/*metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Brain/enzymology/*metabolism ; Brain Ischemia/complications/*metabolism ; Cerebral Infarction/*etiology ; Cerebrovascular Circulation ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Neurons/*enzymology ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase ; Nitroarginine
    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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    Negative selection of precursor thymocytes before their differentiation into CD4+CD8+ cells (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-23
    Description: Thymic selection of the developing T cell repertoire is thought to occur at the CD4+CD8+ stage of differentiation and to be determined by the specificity of the T cell receptors (TCRs) that CD4+CD8+ thymocytes express. However, TCR signals can inhibit the differentiation of precursor thymocytes into CD4+CD8+ cells, which suggests that selection might occur earlier than thought. Indeed, in a negatively selecting male thymus, CD4-CD8lo precursor thymocytes that express a transgenic TCR to male antigen are developmentally arrested as a consequence of antigen encounter and fail to become CD4+CD8+. Thus, negative selection can occur before the CD4+CD8+ stage of differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahama, Y -- Shores, E W -- Singer, A -- New York, N.Y. -- Science. 1992 Oct 23;258(5082):653-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, 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/1357752" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*immunology ; Antigens, CD8/*immunology ; CD4-Positive T-Lymphocytes/cytology/*immunology ; Cell Differentiation/immunology ; Female ; Flow Cytometry ; Male ; Mice ; Mice, Transgenic/immunology ; Receptors, Antigen, T-Cell/*immunology ; T-Lymphocytes/cytology/*immunology ; Thymus Gland/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-07
    Description: A strong candidate for the 17q-linked BRCA1 gene, which influences susceptibility to breast and ovarian cancer, has been identified by positional cloning methods. Probable predisposing mutations have been detected in five of eight kindreds presumed to segregate BRCA1 susceptibility alleles. The mutations include an 11-base pair deletion, a 1-base pair insertion, a stop codon, a missense substitution, and an inferred regulatory mutation. The BRCA1 gene is expressed in numerous tissues, including breast and ovary, and encodes a predicted protein of 1863 amino acids. This protein contains a zinc finger domain in its amino-terminal region, but is otherwise unrelated to previously described proteins. Identification of BRCA1 should facilitate early diagnosis of breast and ovarian cancer susceptibility in some individuals as well as a better understanding of breast cancer biology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miki, Y -- Swensen, J -- Shattuck-Eidens, D -- Futreal, P A -- Harshman, K -- Tavtigian, S -- Liu, Q -- Cochran, C -- Bennett, L M -- Ding, W -- CA-48711/CA/NCI NIH HHS/ -- CA-54936/CA/NCI NIH HHS/ -- CA-55914/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):66-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Informatics, University of Utah Medical Center, Salt Lake City 84132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7545954" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Alternative Splicing ; Amino Acid Sequence ; Animals ; BRCA1 Protein ; Breast Neoplasms/*genetics ; *Chromosomes, Human, Pair 17 ; Female ; *Genes, Tumor Suppressor ; Genetic Predisposition to Disease ; Germ-Line Mutation ; Haplotypes ; Humans ; Lod Score ; Male ; Molecular Sequence Data ; *Mutation ; Neoplasm Proteins/chemistry/*genetics/physiology ; Ovarian Neoplasms/*genetics ; Pedigree ; Phenotype ; Transcription Factors/chemistry/*genetics/physiology ; Zinc Fingers
    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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    A putative ATP-activated Na+ channel involved in sperm-induced fertilization (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-23
    Description: Extracellular application of adenosine triphosphate (ATP) to defolliculated Xenopus laevis oocytes activated a saturating inward current with a maximal amplitude E(max) of 2.4 +/- 0.2 microamperes and an apparent Michaelis constant of 197.6 micromolar. The current was carried predominantly by sodium ions and potently inhibited by amiloride, guanosine triphosphate (GTP), and its nonhydrolyzable analogs guanosine 5'-[beta,gamma-imido]triphosphate (GppNHp) and guanosine 5'-O-(3-thiotriphosphate). Likewise, in vitro fertilization using mature eggs and Xenopus sperm was inhibited by amiloride, GTP, and GppNHp. Hence, an ATP receptor on the egg membrane may be the recipient target for ATP originating in sperm, suggesting that an ATP-induced increase in sodium permeability mediates the initial sperm to egg signal in the fertilization process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kupitz, Y -- Atlas, D -- New York, N.Y. -- Science. 1993 Jul 23;261(5120):484-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Hebrew University of Jerusalem, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8392753" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/analogs & derivatives/pharmacology/*physiology ; Amiloride/pharmacology ; Animals ; Female ; Guanosine Triphosphate/analogs & derivatives/pharmacology ; In Vitro Techniques ; Male ; Membrane Potentials/physiology ; Oocytes/physiology ; Receptors, Purinergic/drug effects/physiology ; Sodium Channels/*physiology ; Sperm-Ovum Interactions/*physiology ; Xenopus laevis
    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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    Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi's sarcoma (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-16
    Description: Representational difference analysis was used to isolate unique sequences present in more than 90 percent of Kaposi's sarcoma (KS) tissues obtained from patients with acquired immunodeficiency syndrome (AIDS). These sequences were not present in tissue DNA from non-AIDS patients, but were present in 15 percent of non-KS tissue DNA samples from AIDS patients. The sequences are homologous to, but distinct from, capsid and tegument protein genes of the Gammaherpesvirinae, herpesvirus saimiri and Epstein-Barr virus. These KS-associated herpesvirus-like (KSHV) sequences appear to define a new human herpesvirus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Y -- Cesarman, E -- Pessin, M S -- Lee, F -- Culpepper, J -- Knowles, D M -- Moore, P S -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1865-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, 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/7997879" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*complications ; Amino Acid Sequence ; Base Composition ; Base Sequence ; Blotting, Southern ; Cloning, Molecular ; DNA, Viral/*analysis/chemistry/genetics ; Female ; Herpesviridae/*genetics ; Herpesvirus 2, Saimiriine/genetics ; Herpesvirus 4, Human/genetics ; Humans ; Male ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Open Reading Frames ; Polymerase Chain Reaction ; Retrospective Studies ; Sarcoma, Kaposi/etiology/*virology ; Sequence Homology, Amino 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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  • 6
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    Mini-mouse: disruption of the pygmy locus in a transgenic insertional mutant (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-23
    Description: A founder transgenic mouse harbored two different integration patterns of a transgene at the same locus, each of which gave rise to a similar autosomal recessive mutation. Mice of the mutant phenotype were of small stature but had normal levels of growth hormone. The disrupted locus was cloned, and a genetic and molecular analysis showed that the insertional mutants were allelic to a spontaneous mutant, pygmy. The mice should be a useful model for the growth hormone-resistant human dwarf syndromes and could lead to a greater understanding of the pathways involved in growth and development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiang, X -- Benson, K F -- Chada, K -- GM38731/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):967-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway 08854.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305264" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/genetics ; Disease Models, Animal ; Dwarfism/*genetics ; Female ; Growth Hormone/blood ; Male ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Mutation ; Nucleic Acid Hybridization ; Pedigree ; Restriction Mapping
    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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    Sexually antagonistic genes: experimental evidence (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-05
    Description: When selection differs between the sexes, a mutation beneficial to one sex may be harmful to the other (sexually antagonistic). Because the sexes share a common gene pool, selection in one sex can interfere with the other's adaptive evolution. Theory predicts that sexually antagonistic mutations should accumulate in tight linkage with a new sex-determining gene, even when the harm to benefit ratio is high. Genetic markers and artificial selection were used to make a pair of autosomal genes segregate like a new pair of sex-determining genes in a Drosophila melanogaster model system. A 29-generation study provides experimental evidence that sexually antagonistic genes may be common in nature and will accumulate in response to a new sex-determining gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rice, W R -- New York, N.Y. -- Science. 1992 Jun 5;256(5062):1436-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biology Board of Studies, University of California, Santa Cruz 95064.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1604317" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila melanogaster/*genetics ; Eye Color/genetics ; Female ; *Genes ; Male ; Phenotype ; *Recombination, Genetic ; *Selection, Genetic ; *Sex Ratio
    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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    Degeneration of a nonrecombining chromosome (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-14
    Description: Comparative studies suggest that sex chromosomes begin as ordinary autosomes that happen to carry a major sex determining locus. Over evolutionary time the Y chromosome is selected to stop recombining with the X chromosome, perhaps in response to accumulation of alleles beneficial to the heterogametic but harmful to the homogametic sex. Population genetic theory predicts that a nonrecombining Y chromosome should degenerate. Here this prediction is tested by application of specific selection pressures to Drosophila melanogaster populations. Results demonstrate the decay of a nonrecombining, nascent Y chromosome and the capacity for recombination to ameliorate such decay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rice, W R -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):230-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, Santa Cruz 95064.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8284674" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crosses, Genetic ; Drosophila melanogaster/*genetics/physiology ; Female ; Haplotypes ; Male ; Mutation ; *Recombination, Genetic ; *Y 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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  • 9
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    Long-range cis preference in DNA homology search over the length of a Drosophila chromosome (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-18
    Description: P element-induced chromosome breakage on the X chromosome of Drosophila melanogaster was repaired six times more frequently when a homologous template was located anywhere on the X chromosome rather than on an autosome. Cis-trans comparisons confirmed that recombinational repair was more frequent when the interacting sequences were physically connected. These results suggest that the search for homology between the broken ends and a matching template sequence occurs preferentially in the cis configuration. This cis advantage operates over more than 15 megabases of DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Engels, W R -- Preston, C R -- Johnson-Schlitz, D M -- GM30948/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1623-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics Department, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128250" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Chromosomes ; DNA/chemistry/*genetics ; *DNA Repair ; DNA Transposable Elements ; Drosophila melanogaster/*genetics ; Female ; *Gene Conversion ; Male ; Molecular Sequence Data ; *Sequence Homology, Nucleic Acid ; Templates, 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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  • 10
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    5-Methylcytosine as an endogenous mutagen in the human LDL receptor and p53 genes (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-14
    Description: Direct genomic sequencing revealed that cytosine residues known to have undergone a germ-line mutation in the low density lipoprotein receptor gene or somatic mutations in the p53 tumor suppressor gene were methylated in all normal human tissues analyzed. Thus, these mutations should be scored as transitions from 5-methylcytosine to thymine rather than from cytosine to thymine. Methylated cytosines occur exclusively at CpG dinucleotides, which, although markedly underrepresented in human DNA, are sites for more than 30 percent of all known disease-related point mutations. Thus, 5-methylcytosine functions as an endogenous mutagen and carcinogen in humans, in that methylation seems to increase the potential for mutation at cytosine residues at least by a factor of 10.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rideout, W M 3rd -- Coetzee, G A -- Olumi, A F -- Jones, P A -- R35 CA49758/CA/NCI NIH HHS/ -- T32 CA09569/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1288-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Urological Cancer Research Laboratory, Kenneth Norris Jr. Comprehensive Cancer Center, University of Southern California, Los Angeles 90033.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1697983" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine ; Base Sequence ; Cytosine/*analogs & derivatives/physiology ; Deoxyribonuclease HpaII ; Deoxyribonucleases, Type II Site-Specific ; Dinucleoside Phosphates/genetics ; Guanosine ; Humans ; Leukocytes ; Male ; Methylation ; Molecular Sequence Data ; *Mutation ; Oncogene Proteins/*genetics ; Phosphoproteins/*genetics ; Polymerase Chain Reaction ; Receptors, LDL/*genetics ; Spermatozoa ; Tumor Suppressor Protein p53
    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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