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  • Female  (4)
  • American Association for the Advancement of Science (AAAS)  (4)
  • Cell Press
  • Periodicals Archive Online (PAO)
  • Springer
  • Springer Nature
  • 1990-1994  (2)
  • 1985-1989  (2)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (4)
  • Cell Press
  • Periodicals Archive Online (PAO)
  • Springer
  • Springer Nature
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  • 1
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    Autoantibodies to glutamate receptor GluR3 in Rasmussen's encephalitis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-29
    Description: Rasmussen's encephalitis is a progressive childhood disease of unknown cause characterized by severe epilepsy, hemiplegia, dementia, and inflammation of the brain. During efforts to raise antibodies to recombinant glutamate receptors (GluRs), behaviors typical of seizures and histopathologic features mimicking Rasmussen's encephalitis were found in two rabbits immunized with GluR3 protein. A correlation was found between the presence of Rasmussen's encephalitis and serum antibodies to GluR3 detected by protein immunoblot analysis and by immunoreactivity to transfected cells expressing GluR3. Repeated plasma exchanges in one seriously ill child transiently reduced serum titers of GluR3 antibodies, decreased seizure frequency, and improved neurologic function. Thus, GluR3 is an autoantigen in Rasmussen's encephalitis, and an autoimmune process may underlie this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogers, S W -- Andrews, P I -- Gahring, L C -- Whisenand, T -- Cauley, K -- Crain, B -- Hughes, T E -- Heinemann, S F -- McNamara, J O -- NS17771/NS/NINDS NIH HHS/ -- NS28709/NS/NINDS NIH HHS/ -- NS30990R29/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):648-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salt Lake City Geriatric Research Education and Clinical Center, Veterans Affairs Medical Center, UT.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Specificity ; Autoantibodies/blood/*immunology ; Brain/pathology ; Cell Line ; Child ; Disease Models, Animal ; Encephalitis/complications/*immunology/pathology/therapy ; Female ; Humans ; Male ; Plasma Exchange ; Rabbits ; Receptors, Glutamate/*immunology ; Recombinant Fusion Proteins/immunology ; Seizures/etiology/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    An experimental study of inbreeding depression in a natural habitat (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: Inbreeding is known to lead to decreased survival and reproduction in captive populations of animals. It is also important to know whether inbreeding has deleterious effects in natural habitats. An estimate was made of the effects of inbreeding in white-footed mice, Peromyscus leucopus noveboracensis, derived from a wild population. This study demonstrates that inbreeding had a significant detrimental effect on the survivorship of mice reintroduced into a natural habitat. This effect was more severe than the effect observed in laboratory studies of the population.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jimenez, J A -- Hughes, K A -- Alaks, G -- Graham, L -- Lacy, R C -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):271-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Illinois-Chicago 60680.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939661" target="_blank"〉PubMed〈/a〉
    Keywords: Analysis of Variance ; Animals ; Body Weight ; Female ; *Inbreeding ; Likelihood Functions ; Male ; Peromyscus/genetics/*physiology ; Regression Analysis ; Survival Rate
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    The gene for familial polyposis coli maps to the long arm of chromosome 5 (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-04
    Description: The inherited genetic defect in adenomatous polyposis has been localized to a small region on the long arm of chromosome 5. Sixteen DNA marker loci were used to construct a linkage map of the chromosome. When five kindreds segregating a gene for adenomatous polyposis coli were characterized with a number of the markers, significant linkage was found between one marker and the disease gene. Linkage analysis determined the location of the defective gene within a primary genetic map of chromosome 5.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leppert, M -- Dobbs, M -- Scambler, P -- O'Connell, P -- Nakamura, Y -- Stauffer, D -- Woodward, S -- Burt, R -- Hughes, J -- Gardner, E -- CA40641/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1411-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Human Genetics, 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/3479843" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; *Chromosomes, Human, Pair 5 ; Colonic Polyps/*genetics ; Female ; Gardner Syndrome/genetics ; *Genes ; Genetic Markers ; Humans ; Lod Score ; Male ; Neoplasms, Multiple Primary/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Point mutations in the human vitamin D receptor gene associated with hypocalcemic rickets (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-23
    Description: Hypocalcemic vitamin D-resistant rickets is a human genetic disease resulting from target organ resistance to the action of 1,25-dihydroxyvitamin D3. Two families with affected children homozygous for this autosomal recessive disorder were studied for abnormalities in the intracellular vitamin D receptor (VDR) and its gene. Although the receptor displays normal binding of 1,25-dihydroxyvitamin D3 hormone, VDR from affected family members has a decreased affinity for DNA. Genomic DNA isolated from these families was subjected to oligonucleotide-primed DNA amplification, and each of the nine exons encoding the receptor protein was sequenced for a genetic mutation. In each family, a different single nucleotide mutation was found in the DNA binding domain of the protein; one family near the tip of the first zinc finger (Gly----Asp) and one at the tip of the second zinc finger (Arg----Gly). The mutant residues were created in vitro by oligonucleotide directed point mutagenesis of wild-type VDR complementary DNA and this cDNA was transfected into COS-1 cells. The produced protein is biochemically indistinguishable from the receptor isolated from patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, M R -- Malloy, P J -- Kieback, D G -- Kesterson, R A -- Pike, J W -- Feldman, D -- O'Malley, B W -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1702-5.〈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/2849209" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Calcitriol/metabolism ; Cell Line ; Cell Line, Transformed ; Codon ; DNA/genetics/metabolism ; Exons ; Female ; Gene Amplification ; Homozygote ; Humans ; Hypocalcemia/*genetics ; Immunoblotting ; Male ; Molecular Sequence Data ; *Mutation ; Receptors, Calcitriol ; Receptors, Steroid/*genetics/metabolism ; Rickets/*genetics ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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