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  • Base Sequence  (42)
  • Adult
  • American Association for the Advancement of Science (AAAS)  (47)
  • 2010-2014
  • 1990-1994  (47)
  • 1980-1984
  • 1940-1944
  • 1990  (47)
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Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (47)
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  • 2010-2014
  • 1990-1994  (47)
  • 1980-1984
  • 1940-1944
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  • 1
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    Identification of a sequence in the PEPCK gene that mediates a negative effect of insulin on transcription (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-03
    Description: Phosphoenolpyruvate carboxykinase (PEPCK) governs the rate-limiting step in gluconeogenesis. Glucocorticoids and adenosine 3',5'-monophosphate (cAMP) increase PEPCK gene transcription and gluconeogenesis, whereas insulin has the opposite effect. Insulin is dominant, since it prevents cAMP and glucocorticoid-stimulated transcription. Glucocorticoid and cAMP response elements have been located in the PEPCK gene and now a 15-base pair insulin-responsive sequence (IRS) is described. Evidence for a binding activity that recognizes this sequence is presented.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, R M -- Lucas, P C -- Forest, C D -- Magnuson, M A -- Granner, D K -- DK 20593/DK/NIDDK NIH HHS/ -- DK 35107/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 3;249(4968):533-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, Vanderbilt University Medical School, Nashville, TN 37232-0615.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2166335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; Cyclic AMP/analogs & derivatives/physiology ; Dexamethasone/pharmacology ; *Genes, Regulator ; Insulin/*pharmacology ; Molecular Sequence Data ; Phosphoenolpyruvate Carboxykinase (GTP)/*genetics/metabolism ; RNA, Messenger/drug effects/genetics ; Recombinant Fusion Proteins/metabolism ; Thionucleotides ; Transcription, Genetic/*drug effects ; 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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  • 2
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    RAG-1 and RAG-2, adjacent genes that synergistically activate V(D)J recombination (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-22
    Description: The vast repertoire of immunoglobulins and T cell receptors is generated, in part, by V(D)J recombination, a series of genomic rearrangements that occur specifically in developing lymphocytes. The recombination activating gene, RAG-1, which is a gene expressed exclusively in maturing lymphoid cells, was previously isolated. RAG-1 inefficiently induced V(D)J recombinase activity when transfected into fibroblasts, but cotransfection with an adjacent gene, RAG-2, has resulted in at least a 1000-fold increase in the frequency of recombination. The 2.1-kilobase RAG-2 complementary DNA encodes a putative protein of 527 amino acids whose sequence is unrelated to that of RAG-1. Like RAG-1, RAG-2 is conserved between species that carry out V(D)J recombination, and its expression pattern correlates precisely with that of V(D)J recombinase activity. In addition to being located just 8 kilobases apart, these convergently transcribed genes are unusual in that most, if not all, of their coding and 3' untranslated sequences are contained in single exons. RAG-1 and RAG-2 might activate the expression of the V(D)J recombinase but, more likely, they directly participate in the recombination reaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oettinger, M A -- Schatz, D G -- Gorka, C -- Baltimore, D -- GM39458/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 22;248(4962):1517-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2360047" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Biological Evolution ; Cattle ; Cell Line ; Chickens ; Cricetinae ; DNA/*genetics ; DNA Nucleotidyltransferases/*genetics ; *DNA-Binding Proteins ; Dogs ; Female ; *Gene Rearrangement, B-Lymphocyte ; *Gene Rearrangement, T-Lymphocyte ; *Homeodomain Proteins ; Humans ; Male ; Mice ; Molecular Sequence Data ; *Multigene Family ; Nuclear Proteins ; Nucleic Acid Hybridization ; Opossums ; Proteins/*genetics ; Rabbits ; Recombination, Genetic/*genetics ; Restriction Mapping ; Transfection ; Turtles ; VDJ Recombinases
    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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    An insertion in the human thyrotropin receptor critical for high affinity hormone binding (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-21
    Description: Thyrotropin (TSH), luteinizing hormone (LH), and chorionic gonadotropin (CG) are structurally related glycoprotein hormones, which bind to receptors that share a high degree of sequence similarity. However, comparison of the primary amino acid sequences of the TSH and LH-CG receptors reveals two unique insertions of 8 and 50 amino acids in the extracellular domain of the TSH receptor. The functional significance of these insertions were determined by site-directed mutagenesis. Deletion of the 50-amino acid tract (residues 317 to 366) had no effect on TSH binding or on TSH and thyroid-stimulating immunoglobulin (TSI) biological activities. In contrast, either deletion or substitution of the eight-amino acid region (residues 38 to 45) abolished these activities. This eight-amino acid tract near the amino terminus of the TSH receptor appears to be an important site of interaction for both TSH and TSI.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wadsworth, H L -- Chazenbalk, G D -- Nagayama, Y -- Russo, D -- Rapoport, B -- DK-19289/DK/NIDDK NIH HHS/ -- DK-36182/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 21;249(4975):1423-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Veterans Administration Medical Center, San Francisco, CA 94121.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2169649" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Cell Line ; Chromosome Deletion ; Clone Cells ; Cyclic AMP/metabolism ; Humans ; Molecular Sequence Data ; Mutation ; Oligonucleotide Probes ; Receptors, Thyrotropin/*genetics/metabolism ; Thyrotropin/*metabolism/pharmacology ; Transfection
    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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    Inheritance of proliferative breast disease in breast cancer kindreds (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-21
    Description: Previous studies have emphasized that genetic susceptibility to breast cancer is rare and is expressed primarily as premenopausal breast cancer, bilateral breast cancer, or both. Proliferative breast disease (PBD) is a significant risk factor for the development of breast cancer and appears to be a precursor lesion. PBD and breast cancer were studied in 103 women from 20 kindreds that were selected for the presence of two first degree relatives with breast cancer and in 31 control women. Physical examination, screening mammography, and four-quadrant fine-needle breast aspirates were performed. Cytologic analysis of breast aspirates revealed PBD in 35% of clinically normal female first degree relatives of breast cancer cases and in 13% of controls. Genetic analysis suggests that genetic susceptibility causes both PBD and breast cancer in these kindreds. This study supports the hypothesis that this susceptibility is responsible for a considerable portion of breast cancer, including unilateral and postmenopausal breast cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skolnick, M H -- Cannon-Albright, L A -- Goldgar, D E -- Ward, J H -- Marshall, C J -- Schumann, G B -- Hogle, H -- McWhorter, W P -- Wright, E C -- Tran, T D -- CA-28854/CA/NCI NIH HHS/ -- CA-42014/CA/NCI NIH HHS/ -- CA-48711/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1715-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Utah Regional Cancer Center, 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/2270486" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Breast Diseases/*genetics/pathology ; Breast Neoplasms/*genetics/pathology ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Menopause ; Middle Aged ; Pedigree
    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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    Mutation of the Alzheimer's disease amyloid gene in hereditary cerebral hemorrhage, Dutch type (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-01
    Description: An amyloid protein that precipitates in the cerebral vessel walls of Dutch patients with hereditary cerebral hemorrhage with amyloidosis is similar to the amyloid protein in vessel walls and senile plaques in brains of patients with Alzheimer's disease, Down syndrome, and sporadic cerebral amyloid angiopathy. Cloning and sequencing of the two exons that encode the amyloid protein from two patients with this amyloidosis revealed a cytosine-to-guanine transversion, a mutation that caused a single amino acid substitution (glutamine instead of glutamic acid) at position 22 of the amyloid protein. The mutation may account for the deposition of this amyloid protein in the cerebral vessel walls of these patients, leading to cerebral hemorrhages and premature death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, E -- Carman, M D -- Fernandez-Madrid, I J -- Power, M D -- Lieberburg, I -- van Duinen, S G -- Bots, G T -- Luyendijk, W -- Frangione, B -- AG 05891/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1124-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, New York University Medical Center, NY 10016.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2111584" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Alleles ; Alzheimer Disease/*genetics ; Amino Acid Sequence ; Amyloid/*genetics ; Amyloid beta-Protein Precursor ; Amyloidosis/complications/*genetics ; Base Sequence ; Brain Chemistry ; Cerebral Hemorrhage/etiology/*genetics ; Cerebrovascular Disorders/complications/*genetics ; Dna ; Deoxyribonucleases, Type II Site-Specific ; Exons ; Female ; Genes, Dominant ; Humans ; Middle Aged ; Molecular Sequence Data ; *Mutation ; Netherlands ; Polymerase Chain Reaction ; Protein Precursors/*genetics
    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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    Messenger RNA transport and HIV rev regulation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, D D -- Sharp, P A -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):614-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2143313" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; *Gene Expression Regulation, Viral ; *Genes, Viral ; *Genes, rev ; HIV/*genetics ; Molecular Sequence Data ; RNA Splicing ; RNA, Messenger/*genetics/metabolism ; Ribonucleoproteins/genetics ; Ribonucleoproteins, Small Nuclear
    Print ISSN: 0036-8075
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  • 7
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    Disruption of the human SCL locus by "illegitimate" V-(D)-J recombinase activity (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-07
    Description: A fusion complementary DNA in the T cell line HSB-2 elucidates a provocative mechanism for the disruption of the putative hematopoietic transcription factor SCL. The fusion cDNA results from an interstitial deletion between a previously unknown locus, SIL (SCL interrupting locus), and the 5' untranslated region of SCL. Similar to 1;14 translocations, this deletion disrupts the SCL 5' regulatory region. This event is probably mediated by V-(D)-J recombinase activity, although neither locus is an immunoglobulin or a T cell receptor. Two other T cell lines, CEM and RPMI 8402, have essentially identical deletions. Thus, in lymphocytes, growth-affecting genes other than immune receptors risk rearrangements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aplan, P D -- Lombardi, D P -- Ginsberg, A M -- Cossman, J -- Bertness, V L -- Kirsch, I R -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1426-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute-Navy Medical Oncology Branch, Naval Hospital, Bethesda, MD 20889-5105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2255914" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Basic Helix-Loop-Helix Transcription Factors ; Cell Line ; Chromosome Deletion ; DNA Nucleotidyltransferases/*metabolism ; DNA-Binding Proteins/genetics ; Exons ; *Gene Rearrangement ; Humans ; Molecular Sequence Data ; Oligonucleotide Probes ; Plasmids ; Proto-Oncogene Proteins/genetics ; Restriction Mapping ; Sequence Homology, Nucleic Acid ; T-Lymphocytes ; Transcription Factors/*genetics ; VDJ Recombinases
    Print ISSN: 0036-8075
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  • 8
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    Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-10
    Description: Familial cancer syndromes have helped to define the role of tumor suppressor genes in the development of cancer. The dominantly inherited Li-Fraumeni syndrome (LFS) is of particular interest because of the diversity of childhood and adult tumors that occur in affected individuals. The rarity and high mortality of LFS precluded formal linkage analysis. The alternative approach was to select the most plausible candidate gene. The tumor suppressor gene, p53, was studied because of previous indications that this gene is inactivated in the sporadic (nonfamilial) forms of most cancers that are associated with LFS. Germ line p53 mutations have been detected in all five LFS families analyzed. These mutations do not produce amounts of mutant p53 protein expected to exert a trans-dominant loss of function effect on wild-type p53 protein. The frequency of germ line p53 mutations can now be examined in additional families with LFS, and in other cancer patients and families with clinical features that might be attributed to the mutation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malkin, D -- Li, F P -- Strong, L C -- Fraumeni, J F Jr -- Nelson, C E -- Kim, D H -- Kassel, J -- Gryka, M A -- Bischoff, F Z -- Tainsky, M A -- 34936/PHS HHS/ -- 5-T32-CA09299/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1233-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Genetics, Massachusetts General Hospital Cancer Center, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1978757" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Breast Neoplasms/*genetics ; Chromosomes, Human, Pair 17 ; Cloning, Molecular ; Codon ; DNA/genetics ; Deoxyribonucleases, Type II Site-Specific ; *Genes, p53 ; Genetic Testing ; Germ Cells ; Humans ; Molecular Sequence Data ; *Mutation ; Neoplastic Syndromes, Hereditary/*genetics ; Pedigree ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Repetitive Sequences, Nucleic Acid ; Sarcoma/*genetics ; Tumor Suppressor Protein p53/genetics
    Print ISSN: 0036-8075
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  • 9
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    Detection of Borrelia burgdorferi DNA in museum specimens of Ixodes dammini ticks (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-21
    Description: In order to investigate the potential for Borrelia burgdorferi infection before the recognition of Lyme disease as a clinical entity, the polymerase chain reaction (PCR) was used to examine museum specimens of Ixodes dammini (deer ticks) for the presence of spirochete-specific DNA sequences. One hundred and thirty-six archival tick specimens were obtained representing various continental U.S. locations; DNA sequences characteristic of modern day isolates of B. burgdorferi were detected in 13 1940s specimens from Montauk Point and Hither Hills, Long Island, New York. Five archival specimens of Dermacentor variabilis (dog tick) from the same collection and 118 Ixodes specimens from other endemic and nonendemic sites were negative. These data suggest that the appearance of the Lyme disease spirochete in suitable arthropod vectors preceded, by at least a generation, the formal recognition of this disease as a clinical entity in the United States.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Persing, D H -- Telford, S R 3rd -- Rys, P N -- Dodge, D E -- White, T J -- Malawista, S E -- Spielman, A -- AM07107/AM/NIADDK NIH HHS/ -- AM10493/AM/NIADDK NIH HHS/ -- AM40452/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Sep 21;249(4975):1420-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2402635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Borrelia burgdorferi Group/genetics/*isolation & purification ; DNA, Bacterial/genetics/*isolation & purification ; Dogs ; Genes, Bacterial ; Humans ; Lyme Disease/microbiology ; Molecular Sequence Data ; Museums ; New York ; Ticks/*microbiology
    Print ISSN: 0036-8075
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  • 10
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    Bacterial origin of a chloroplast intron: conserved self-splicing group I introns in cyanobacteria (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-14
    Description: A self-splicing group I intron has been found in the gene for a leucine transfer RNA in two species of Anabaena, a filamentous nitrogen-fixing cyanobacterium. The intron is similar to one that is found at the identical position in the same transfer RNA gene of chloroplasts of land plants. Because cyanobacteria were the progenitors of chloroplasts, it is likely that group I introns predated the endosymbiotic association of these eubacteria with eukaryotic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, M Q -- Kathe, S D -- Goodrich-Blair, H -- Nierzwicki-Bauer, S A -- Shub, D A -- GM37746/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 14;250(4987):1566-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, State University of New York, Albany 12222.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2125747" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/*genetics ; Base Sequence ; Biological Evolution ; Chloroplasts/*metabolism ; Cyanobacteria/*genetics ; DNA/genetics/metabolism ; Deoxyribonuclease EcoRI/metabolism ; Deoxyribonuclease HindIII/metabolism ; Introns/*genetics ; Molecular Sequence Data ; Nucleic Acid Conformation ; *RNA Splicing ; RNA, Transfer, Leu/*genetics ; Restriction Mapping ; Tetrahymena/genetics
    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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