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  • Humans  (93)
  • Amino Acid Sequence  (68)
  • 1995-1999  (138)
  • 1980-1984
  • 1970-1974
  • 1940-1944
  • 1995  (138)
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  • 1995-1999  (138)
  • 1980-1984
  • 1970-1974
  • 1940-1944
Year
  • 1
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    An STS-based map of the human genome (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-12-22
    Description: A physical map has been constructed of the human genome containing 15,086 sequence-tagged sites (STSs), with an average spacing of 199 kilobases. The project involved assembly of a radiation hybrid map of the human genome containing 6193 loci and incorporated a genetic linkage map of the human genome containing 5264 loci. This information was combined with the results of STS-content screening of 10,850 loci against a yeast artificial chromosome library to produce an integrated map, anchored by the radiation hybrid and genetic maps. The map provides radiation hybrid coverage of 99 percent and physical coverage of 94 percent of the human genome. The map also represents an early step in an international project to generate a transcript map of the human genome, with more than 3235 expressed sequences localized. The STSs in the map provide a scaffold for initiating large-scale sequencing of the human genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hudson, T J -- Stein, L D -- Gerety, S S -- Ma, J -- Castle, A B -- Silva, J -- Slonim, D K -- Baptista, R -- Kruglyak, L -- Xu, S H -- Hu, X -- Colbert, A M -- Rosenberg, C -- Reeve-Daly, M P -- Rozen, S -- Hui, L -- Wu, X -- Vestergaard, C -- Wilson, K M -- Bae, J S -- Maitra, S -- Ganiatsas, S -- Evans, C A -- DeAngelis, M M -- Ingalls, K A -- Nahf, R W -- Horton, L T Jr -- Anderson, M O -- Collymore, A J -- Ye, W -- Kouyoumjian, V -- Zemsteva, I S -- Tam, J -- Devine, R -- Courtney, D F -- Renaud, M T -- Nguyen, H -- O'Connor, T J -- Fizames, C -- Faure, S -- Gyapay, G -- Dib, C -- Morissette, J -- Orlin, J B -- Birren, B W -- Goodman, N -- Weissenbach, J -- Hawkins, T L -- Foote, S -- Page, D C -- Lander, E S -- HG00017/HG/NHGRI NIH HHS/ -- HG00098/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1995 Dec 22;270(5244):1945-54.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead-MIT Center for Genome Research, Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8533086" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Chromosome Mapping ; Chromosomes, Artificial, Yeast ; Databases, Factual ; Gene Expression ; Genetic Markers ; *Genome, Human ; *Human Genome Project ; Humans ; Hybrid Cells ; Polymerase Chain Reaction ; *Sequence Analysis, DNA ; *Sequence Tagged Sites
    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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    Genomic structure of an attenuated quasi species of HIV-1 from a blood transfusion donor and recipients (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-11-10
    Description: A blood donor infected with human immunodeficiency virus-type 1 (HIV-1) and a cohort of six blood or blood product recipients infected from this donor remain free of HIV-1-related disease with stable and normal CD4 lymphocyte counts 10 to 14 years after infection. HIV-1 sequences from either virus isolates or patient peripheral blood mononuclear cells had similar deletions in the nef gene and in the region of overlap of nef and the U3 region of the long terminal repeat (LTR). Full-length sequencing of one isolate genome and amplification of selected HIV-1 genome regions from other cohort members revealed no other abnormalities of obvious functional significance. These data show that survival after HIV infection can be determined by the HIV genome and support the importance of nef or the U3 region of the LTR in determining the pathogenicity of HIV-1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deacon, N J -- Tsykin, A -- Solomon, A -- Smith, K -- Ludford-Menting, M -- Hooker, D J -- McPhee, D A -- Greenway, A L -- Ellett, A -- Chatfield, C -- Lawson, V A -- Crowe, S -- Maerz, A -- Sonza, S -- Learmont, J -- Sullivan, J S -- Cunningham, A -- Dwyer, D -- Dowton, D -- Mills, J -- New York, N.Y. -- Science. 1995 Nov 10;270(5238):988-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉AIDS Molecular Biology Unit, Macfarlane Burnet Centre for Medical Research, Fairfield, Victoria, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7481804" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Base Composition ; Base Sequence ; *Blood Donors ; Blood Transfusion ; CD4 Lymphocyte Count ; Cohort Studies ; Disease Progression ; Female ; Gene Rearrangement ; *Genes, nef ; Genome, Viral ; HIV Infections/immunology/transmission/*virology ; *HIV Long Terminal Repeat ; HIV-1/*genetics/*pathogenicity/physiology ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; Multigene Family ; Sequence Deletion ; Virulence ; Virus Replication
    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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    Aberrant subcellular localization of BRCA1 in breast cancer (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-11-03
    Description: The BRCA1 gene product was identified as a 220-kilodalton nuclear phosphoprotein in normal cells, including breast ductal epithelial cells, and in 18 of 20 tumor cell lines derived from tissues other than breast and ovary. In 16 of 17 breast and ovarian cancer lines and 17 of 17 samples of cells obtained from malignant effusions, however, BRCA1 localized mainly in cytoplasm. Absence of BRCA1 or aberrant subcellular location was also observed to a variable extent in histological sections of many breast cancer biopsies. These findings suggest that BRCA1 abnormalities may be involved in the pathogenesis of many breast cancers, sporadic as well as familial.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Y -- Chen, C F -- Riley, D J -- Allred, D C -- Chen, P L -- Von Hoff, D -- Osborne, C K -- Lee, W H -- CA58318/CA/NCI NIH HHS/ -- EY05758/EY/NEI NIH HHS/ -- P50CA58183/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Nov 3;270(5237):789-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular Medicine/Institute of Biotechnology, University of Texas Health Science Center at San Antonio 78245, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7481765" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; BRCA1 Protein ; Base Sequence ; Breast/*chemistry ; Breast Neoplasms/*chemistry/ultrastructure ; Cell Fractionation ; Cell Line ; Cell Nucleus/chemistry ; Cytoplasm/*chemistry ; Female ; Humans ; Male ; Molecular Sequence Data ; Mutation ; Neoplasm Proteins/*analysis/genetics/metabolism ; Neoplasms/chemistry/ultrastructure ; Ovarian Neoplasms/chemistry/ultrastructure ; Pleural Effusion, Malignant/chemistry/pathology ; Transcription Factors/*analysis/genetics/metabolism ; Tumor Cells, Cultured
    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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  • 4
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    Liposomes revisited (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lasic, D D -- Papahadjopoulos, D -- New York, N.Y. -- Science. 1995 Mar 3;267(5202):1275-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MegaBios Corporation, Burlingame, CA 94010.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7871422" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Doxorubicin/administration & dosage ; *Drug Carriers ; *Genetic Therapy ; Humans ; Lipid Bilayers/chemistry ; *Liposomes/chemistry/pharmacokinetics ; Neoplasms/drug therapy ; Transfection
    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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    Activation of a G protein complex by aggregation of beta-1,4-galactosyltransferase on the surface of sperm (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-09-22
    Description: Fertilization is initiated by the species-specific binding of sperm to the extracellular coat of the egg. One sperm receptor for the mouse egg is beta-1,4-galactosyltransferase (GalTase), which binds O-linked oligosaccharides on the egg coat glycoprotein ZP3. ZP3 binding induces acrosomal exocytosis through the activation of a pertussis toxin-sensitive heterotrimeric guanine nucleotide-binding protein (G protein). The cytoplasmic domain of sperm surface GalTase bound to and activated a heterotrimeric G protein complex that contained the Gi alpha subunit. Aggregation of GalTase by multivalent ligands elicited G protein activation. Sperm from transgenic mice that overexpressed GalTase had higher rates of G protein activation than did wild-type sperm, which rendered transgenic sperm hypersensitive to their ZP3 ligand. Thus, the cytoplasmic domain of cell surface GalTase appears to enable it to function as a signal-transducing receptor for extracellular oligosaccharide ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gong, X -- Dubois, D H -- Miller, D J -- Shur, B D -- R01 HD22590/HD/NICHD NIH HHS/ -- R01 HD23479/HD/NICHD NIH HHS/ -- T32 HD07324/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Sep 22;269(5231):1718-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7569899" target="_blank"〉PubMed〈/a〉
    Keywords: Acrosome/physiology ; Adenosine Diphosphate Ribose/metabolism ; Amino Acid Sequence ; Animals ; Cell Membrane/enzymology/metabolism ; Egg Proteins/*metabolism ; GTP-Binding Proteins/*metabolism ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Ligands ; Male ; Membrane Glycoproteins/*metabolism ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; N-Acetyllactosamine Synthase/*metabolism ; Peptide Fragments/metabolism ; Pertussis Toxin ; *Receptors, Cell Surface ; Signal Transduction ; Spermatozoa/enzymology/*metabolism ; Virulence Factors, Bordetella/pharmacology ; Zona Pellucida/*chemistry
    Print ISSN: 0036-8075
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  • 6
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    Inhibition of transcription elongation by the VHL tumor suppressor protein (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-09-08
    Description: Germline mutations in the von Hippel-Lindau tumor suppressor gene (VHL) predispose individuals to a variety of tumors, including renal carcinoma, hemangioblastoma of the central nervous system, and pheochromocytoma. Here, a cellular transcription factor, Elongin (SIII), is identified as a functional target of the VHL protein. Elongin (SIII) is a heterotrimer consisting of a transcriptionally active subunit (A) and two regulatory subunits (B and C) that activate transcription elongation by RNA polymerase II. The VHL protein was shown to bind tightly and specifically to the Elongin B and C subunits and to inhibit Elongin (SIII) transcriptional activity in vitro. These findings reveal a potentially important transcriptional regulatory network in which the VHL protein may play a key role.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duan, D R -- Pause, A -- Burgess, W H -- Aso, T -- Chen, D Y -- Garrett, K P -- Conaway, R C -- Conaway, J W -- Linehan, W M -- Klausner, R D -- GM41628/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1995 Sep 8;269(5229):1402-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Urologic Oncology Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7660122" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cloning, Molecular ; Gene Expression Regulation ; *Genes, Tumor Suppressor ; HeLa Cells ; Humans ; *Ligases ; Molecular Sequence Data ; Mutation ; Nuclear Proteins/genetics/*metabolism ; RNA Polymerase II/metabolism ; Recombinant Proteins/metabolism ; Transcription Factors/chemistry/isolation & purification/*metabolism ; *Transcription, Genetic ; *Tumor Suppressor Proteins ; *Ubiquitin-Protein Ligases ; Von Hippel-Lindau Tumor Suppressor Protein ; von Hippel-Lindau Disease/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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    Adaptive evolution of color vision genes in higher primates (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-09-01
    Description: The intron 4 sequences of the three polymorphic alleles at the X-linked color photo-pigment locus in the squirrel monkey and the marmoset reveal that the alleles in each species are exceptionally divergent. The data further suggest either that each triallelic system has arisen independently in these two New World monkey lineages, or that in each species at least seven deletions and insertions (14 in the two species) in intron 4 have been transferred and homogenized among the alleles by gene conversion or recombination. In either case, the alleles in each species apparently have persisted more than 5 million years and probably have been maintained by overdominant selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shyue, S K -- Hewett-Emmett, D -- Sperling, H G -- Hunt, D M -- Bowmaker, J K -- Mollon, J D -- Li, W H -- EY10317/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1995 Sep 1;269(5228):1265-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics Center, School of Public Health, University of Texas, Houston 77225, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7652574" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Amino Acid Sequence ; Animals ; *Biological Evolution ; Callithrix ; Color Perception/*genetics ; Eye Proteins/*genetics ; Gene Conversion ; Genetic Linkage ; Humans ; Introns ; Male ; Molecular Sequence Data ; Recombination, Genetic ; Repetitive Sequences, Nucleic Acid ; Retinal Pigments/*genetics ; Rod Opsins ; Saimiri ; Sequence Deletion ; Species Specificity ; X Chromosome
    Print ISSN: 0036-8075
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  • 8
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    Impaired energy homeostasis in C/EBP alpha knockout mice (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-08-25
    Description: Mice homozygous for the targeted deletion of the c/ebp alpha gene, which expresses the CCAAT/enhancer-binding protein alpha (C/EBP alpha), did not store hepatic glycogen and died from hypoglycemia within 8 hours after birth. In these mutant mice, the amounts of glycogen synthase messenger RNA were 50 to 70 percent of normal and the transcriptional induction of the genes for two gluconeogenic enzymes, phosphoenolpyruvate carboxykinase and glucose-6-phosphatase, was delayed. The hepatocytes and adipocytes of the mutant mice failed to accumulate lipid and the expression of the gene for uncoupling protein, the defining marker of brown adipose tissue, was reduced. This study demonstrates that C/EBP alpha is critical for the establishment and maintenance of energy homeostasis in neonates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, N D -- Finegold, M J -- Bradley, A -- Ou, C N -- Abdelsayed, S V -- Wilde, M D -- Taylor, L R -- Wilson, D R -- Darlington, G J -- DK 45285/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1995 Aug 25;269(5227):1108-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7652557" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Adipose Tissue, Brown/metabolism ; Animals ; Animals, Newborn ; Blood Glucose/metabolism ; CCAAT-Enhancer-Binding Proteins ; Carrier Proteins/genetics ; DNA-Binding Proteins/genetics/*physiology ; *Energy Metabolism ; Female ; Gene Expression Regulation ; Glucose-6-Phosphatase/genetics ; Glycogen Synthase/genetics/metabolism ; Homeostasis ; Humans ; Ion Channels ; Lipid Metabolism ; Liver/metabolism ; Liver Glycogen/metabolism ; Male ; Membrane Proteins/genetics ; Mice ; Mice, Knockout ; Mitochondrial Proteins ; Nuclear Proteins/genetics/*physiology ; Phosphoenolpyruvate Carboxykinase (GTP)/genetics ; RNA, Messenger/metabolism ; Serum Albumin/genetics
    Print ISSN: 0036-8075
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  • 9
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    Candidate gene for the chromosome 1 familial Alzheimer's disease locus (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-08-18
    Description: A candidate gene for the chromosome 1 Alzheimer's disease (AD) locus was identified (STM2). The predicted amino acid sequence for STM2 is homologous to that of the recently cloned chromosome 14 AD gene (S182). A point mutation in STM2, resulting in the substitution of an isoleucine for an asparagine (N141l), was identified in affected people from Volga German AD kindreds. This N141l mutation occurs at an amino acid residue that is conserved in human S182 and in the mouse S182 homolog. The presence of missense mutations in AD subjects in two highly similar genes strongly supports the hypothesis that mutations in both are pathogenic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy-Lahad, E -- Wasco, W -- Poorkaj, P -- Romano, D M -- Oshima, J -- Pettingell, W H -- Yu, C E -- Jondro, P D -- Schmidt, S D -- Wang, K -- AG0513C/AG/NIA NIH HHS/ -- R01-AG11762/AG/NIA NIH HHS/ -- R01-AG11899/AG/NIA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Aug 18;269(5226):973-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geriatric Research Education, and Clinical Center (182B), Veterans Affairs Medical Center, Seattle, WA 98108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7638622" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Alzheimer Disease/ethnology/*genetics ; Amino Acid Sequence ; Base Sequence ; Chromosome Mapping ; Chromosomes, Human, Pair 1/*genetics ; Cloning, Molecular ; DNA, Complementary/genetics ; Female ; Gene Expression ; Germany/ethnology ; Humans ; Lod Score ; Male ; Membrane Proteins/chemistry/*genetics ; Middle Aged ; Molecular Sequence Data ; Mutation ; Pedigree ; Point Mutation ; Presenilin-2
    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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    Quantitative trait locus for reading disability: correction (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-16
    Description: In the news article "Can risky mergers save hospital-based research?" by Wade Roush (19 May, p. 968), the statement that University Hospitals of Cleveland rose from 20th in the rankings of teaching hospitals funded by the National Institutes of Health (NIH) in 1991 to 12th at present was incorrect. In fact, it was Case Western Reserve University (CWRU), with which University Hospitals of Cleveland is affiliated, that received $69 million in NIH grants in 1993, making it the 20th largest recipient of such grants among medical centers; the university then received $97 million in 1994, raising its rank to 12th. About $15 million of the increase, or 53%, was attributable to CWRU's 1992 affiliation with Henry Ford Hospital in Detroit. Other hospitals affiliated with Case Western include MetroHealth Medical Center, Mount Sinai Medical Center, St. Luke's Medical Center, and Cleveland Veterans' Affairs Medical Center.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cardon, L R -- Smith, S D -- Fulker, D W -- Kimberling, W J -- Pennington, B F -- DeFries, J C -- New York, N.Y. -- Science. 1995 Jun 16;268(5217):1553.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7777847" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; *Chromosomes, Human, Pair 6 ; Diseases in Twins/*genetics ; Dyslexia/*genetics ; Genetic Markers ; Humans ; Twins, Dizygotic ; Twins, Monozygotic
    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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