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  • Articles  (76)
  • Cells, Cultured
  • 1995-1999  (43)
  • 1980-1984  (33)
  • 1935-1939
  • 1930-1934
  • 1920-1924
  • 1996  (43)
  • 1984  (33)
  • Physics  (76)
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  • Articles  (76)
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  • 1995-1999  (43)
  • 1980-1984  (33)
  • 1935-1939
  • 1930-1934
  • 1920-1924
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  • 1
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    IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. An inhibitory form of IRS-1 was observed in muscle and fat tissues from obese rats. These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hotamisligil, G S -- Peraldi, P -- Budavari, A -- Ellis, R -- White, M F -- Spiegelman, B M -- DK 42539/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):665-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571133" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*metabolism ; Adipose Tissue/metabolism ; Animals ; Cells, Cultured ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance/*physiology ; Male ; Mice ; Muscle, Skeletal/metabolism ; Obesity/*metabolism ; Phosphoproteins/metabolism/*physiology ; Phosphorylation ; Rats ; Rats, Zucker ; Receptor, Insulin/*antagonists & inhibitors/metabolism ; Serine/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/*pharmacology
    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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    HIV-1 Langerhans' cell tropism associated with heterosexual transmission of HIV (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: Heterosexual transmission by vaginal intercourse accounts for most transmission of human immunodeficiency virus-type 1 (HIV-1) in Africa and Asia but is less important in the HIV-1 epidemics of the United States and Western Europe. Epithelial Langerhans' cells (LCs) represent a possible source of initial cell contact for vaginal infection. Fifteen primary isolates of HIV-1 from U.S. homosexuals and 18 HIV-1 isolates from Thailand heterosexuals were evaluated for growth in LCs of U.S. origin. All the viruses from the Thai heterosexuals, which were subtype E, grew more efficiently in the LCs than any of the viruses from the U.S. homosexuals, which are subtype B. These results suggest that LC tropism is associated with the efficiency of heterosexual transmission of HIV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soto-Ramirez, L E -- Renjifo, B -- McLane, M F -- Marlink, R -- O'Hara, C -- Sutthent, R -- Wasi, C -- Vithayasai, P -- Vithayasai, V -- Apichartpiyakul, C -- Auewarakul, P -- Pena Cruz, V -- Chui, D S -- Osathanondh, R -- Mayer, K -- Lee, T H -- Essex, M -- 5 D43 TW0004/TW/FIC NIH HHS/ -- CA 39805/CA/NCI NIH HHS/ -- HL 33774/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1291-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard AIDS Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638113" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cells, Cultured ; HIV Core Protein p24/analysis ; HIV Infections/*transmission/virology ; HIV-1/classification/*growth & development/isolation & purification ; Homosexuality, Male ; Humans ; Langerhans Cells/*virology ; Macrophages/virology ; Male ; Monocytes/virology ; *Sexual Behavior ; Sexually Transmitted Diseases, Viral/*transmission/virology ; T-Lymphocytes/virology ; Thailand ; United States ; 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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    Abnormal centrosome amplification in the absence of p53 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: The centrosome plays a vital role in mitotic fidelity, ensuring establishment of bipolar spindles and balanced chromosome segregation. Centrosome duplication occurs only once during the cell cycle and is therefore highly regulated. Here, it is shown that in mouse embryonic fibroblasts (MEFs) lacking the p53 tumor suppressor protein, multiple copies of functionally competent centrosomes are generated during a single cell cycle. In contrast, MEFs prepared from normal mice or mice deficient in the retinoblastoma tumor suppressor gene product do not display these abnormalities. The abnormally amplified centrosomes profoundly affect mitotic fidelity, resulting in unequal segregation of chromosomes. These observations implicate p53 in the regulation of centrosome duplication and suggest one possible mechanism by which the loss of p53 may cause genetic instability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukasawa, K -- Choi, T -- Kuriyama, R -- Rulong, S -- Vande Woude, G F -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1744-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD 21702-1201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood ; Cells, Cultured ; Centrosome/*metabolism ; Culture Media ; Fibroblasts ; Genes, Retinoblastoma ; Genes, p53 ; *Interphase ; Mice ; *Mitosis ; Spindle Apparatus/metabolism/ultrastructure ; Tumor Suppressor Protein p53/*physiology
    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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    Antigen presentation and T cell development in H2-M-deficient mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: HLA-DM (DM) facilitates peptide loading of major histocompatibility complex class II molecules in human cell lines. Mice lacking functional H2-M, the mouse equivalent of DM, have normal amounts of class II molecules at the cell surface, but most of these are associated with invariant chain-derived CLIP peptides. These mice contain large numbers of CD4+ T cells, which is indicative of positive selection in the thymus. Their CD4+ cells were unresponsive to self H2-M-deficient antigen-presenting cells (APCs) but were hyperreactive to wild-type APCs. H2-M-deficient APCs failed to elicit proliferative responses from wild-type T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fung-Leung, W P -- Surh, C D -- Liljedahl, M -- Pang, J -- Leturcq, D -- Peterson, P A -- Webb, S R -- Karlsson, L -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1278-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638109" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigen-Presenting Cells/*immunology ; Antigens, Differentiation, B-Lymphocyte/immunology/metabolism ; Base Sequence ; CD4-Positive T-Lymphocytes/*immunology ; Cells, Cultured ; Gene Targeting ; Histocompatibility Antigens Class II/genetics/*immunology/metabolism ; Isoantigens/immunology ; Lymphocyte Activation ; Mice ; Molecular Sequence Data ; Mutation
    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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  • 5
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    Spread of synaptic depression mediated by presynaptic cytoplasmic signaling (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: Postsynaptic activity may modulate presynaptic functions by transsynaptic retrograde signals. At developing neuromuscular synapses in Xenopus nerve-muscle cultures, a brief increase in the cytosolic calcium ion (Ca2+) concentration in postsynaptic myocytes induced persistent depression of presynaptic transmitter secretion. This depression spread to distant synapses formed by the same neuron. Clearance of extracellular fluid did not prevent the spread of depression, and depression could not be induced by increasing the Ca2+ concentration in a nearby myocyte not in contact with the presynaptic neuron. Thus, the spread of depression is mediated by signaling in the presynaptic cytoplasm, rather than by a retrograde factor in the extracellular space.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cash, S -- Zucker, R S -- Poo, M M -- NS15114/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 May 17;272(5264):998-1001.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York 10027, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638143" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Cells, Cultured ; Chelating Agents ; Cytoplasm/*metabolism ; Egtazic Acid/analogs & derivatives ; Evoked Potentials ; Muscles/cytology/innervation/physiology ; Neurites/physiology ; Neuromuscular Junction/metabolism/*physiology ; Photolysis ; Presynaptic Terminals/physiology ; *Signal Transduction ; Synapses/*physiology ; *Synaptic Transmission ; Ultraviolet Rays ; Xenopus
    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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  • 6
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    Selective activation of NF-kappa B by nerve growth factor through the neurotrophin receptor p75 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-26
    Description: Nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) selectively bind to distinct members of the Trk family of tyrosine kinase receptors, but all three bind with similar affinities to the neurotrophin receptor p75 (p75NTR). The biological significance of neurotrophin binding to p75NTR in cells that also express Trk receptors has been difficult to ascertain. In the absence of TrkA, NGF binding to p75NGR activated the transcription factor nuclear factor kappa B (NF-kappa B) in rat Schwann cells. This activation was not observed in Schwann cells isolated from mice that lacked p75NTR. The effect was selective for NGF; NF-kappa B was not activated by BDNF or NT-3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carter, B D -- Kaltschmidt, C -- Kaltschmidt, B -- Offenhauser, N -- Bohm-Matthaei, R -- Baeuerle, P A -- Barde, Y A -- New York, N.Y. -- Science. 1996 Apr 26;272(5261):542-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiochemistry, Max-Planck Institute for Psychiatry, Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614802" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain-Derived Neurotrophic Factor ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA/metabolism ; L Cells (Cell Line) ; Mice ; Molecular Sequence Data ; NF-kappa B/*metabolism ; Nerve Growth Factors/*metabolism/pharmacology ; Nerve Tissue Proteins/metabolism/pharmacology ; Neurotrophin 3 ; Proto-Oncogene Proteins/metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Nerve Growth Factor ; Receptor, trkA ; Receptors, Nerve Growth Factor/*metabolism ; Schwann Cells/*metabolism ; Signal Transduction/*physiology
    Print ISSN: 0036-8075
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  • 7
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    Binding of APC to the human homolog of the Drosophila discs large tumor suppressor protein (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: The adenomatous polyposis coli gene (APC) is mutated in familial adenomatous polyposis and in sporadic colorectal tumors, and its product binds to the adherens junction protein beta-catenin. Overexpression of APC blocks cell cycle progression. The APC-beta-catenin complex was shown to bind to DLG, the human homolog of the Drosophila discs large tumor suppressor protein. This interaction required the carboxyl-terminal region of APC and the DLG homology repeat region of DLG. APC colocalized with DLG at the lateral cytoplasm in rat colon epithelial cells and at the synapse in cultured hippocampal neurons. These results suggest that the APC-DLG complex may participate in regulation of both cell cycle progression and neuronal function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsumine, A -- Ogai, A -- Senda, T -- Okumura, N -- Satoh, K -- Baeg, G H -- Kawahara, T -- Kobayashi, S -- Okada, M -- Toyoshima, K -- Akiyama, T -- New York, N.Y. -- Science. 1996 May 17;272(5264):1020-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncogene Research, Institute for Microbial Diseases, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638125" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Amino Acid Sequence ; Animals ; Cell Cycle ; Cells, Cultured ; Colon/chemistry/cytology ; Cytoskeletal Proteins/analysis/chemistry/*metabolism ; Drosophila ; *Drosophila Proteins ; Epithelial Cells ; Epithelium/chemistry ; Fluorescent Antibody Technique ; Hippocampus/chemistry/cytology ; Humans ; Insect Hormones/analysis/chemistry/*metabolism ; Mice ; Molecular Sequence Data ; Neurons/chemistry/cytology ; Protein Binding ; Recombinant Fusion Proteins/metabolism ; Synapses/chemistry ; *Trans-Activators ; *Tumor Suppressor Proteins ; beta Catenin
    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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  • 8
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    Fertile results: bringing up baby (eggs) (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):594-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571119" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Culture Techniques ; Cells, Cultured ; Female ; Fertilization in Vitro ; Granulosa Cells/cytology/*physiology ; Mice ; Oocytes/cytology/*physiology ; *Oogenesis ; Organ Culture Techniques ; Ovary/physiology
    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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    Identification of a committed precursor for the mast cell lineage (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-09
    Description: Mast cells originate from hematopoietic stem cells, but the mast cell-committed precursor has not been identified. In the study presented here, a cell population in murine fetal blood that fulfills the criteria of progenitor mastocytes was identified. It is defined by the phenotype Thy-1loc-Kithi, contains cytoplasmic granules, and expresses RNAs encoding mast cell-associated proteases but lacks expression of the high-affinity immunoglobulin E receptor. Thy-1loc-Kithi cells generated functionally competent mast cells at high frequencies in vitro but lacked developmental potential for other hematopoietic lineages. When transferred intraperitoneally, this population reconstituted the peritoneal mast cell compartment of genetically mast cell-deficient W/Wv mice to wild-type levels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodewald, H R -- Dessing, M -- Dvorak, A M -- Galli, S J -- AI-33372/AI/NIAID NIH HHS/ -- AI/CA-23990/AI/NIAID NIH HHS/ -- CA/AI-72074/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):818-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8629001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Thy-1/analysis ; Base Sequence ; Cell Lineage ; Cell Transplantation ; Cells, Cultured ; Cytoplasmic Granules/ultrastructure ; Endopeptidases/genetics/metabolism ; Fetal Blood ; Hematopoietic Stem Cells/*cytology/physiology/ultrastructure ; Immunophenotyping ; Interleukin-3/pharmacology ; Mast Cells/*cytology/physiology/ultrastructure ; Mice ; Molecular Sequence Data ; Peritoneal Cavity/cytology ; Proto-Oncogene Proteins c-kit/analysis ; RNA, Messenger/genetics/metabolism ; Receptors, IgE/analysis/genetics ; Stem Cell Factor/pharmacology
    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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  • 10
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    Cholesterol modification of hedgehog signaling proteins in animal development (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-11
    Description: Hedgehog (Hh) proteins comprise a family of secreted signaling molecules essential for patterning a variety of structures in animal embryogenesis. During biosynthesis, Hh undergoes an autocleavage reaction, mediated by its carboxyl-terminal domain, that produces a lipid-modified amino-terminal fragment responsible for all known Hh signaling activity. Here it is reported that cholesterol is the lipophilic moiety covalently attached to the amino-terminal signaling domain during autoprocessing and that the carboxyl-terminal domain acts as an intramolecular cholesterol transferase. This use of cholesterol to modify embryonic signaling proteins may account for some of the effects of perturbed cholesterol biosynthesis on animal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porter, J A -- Young, K E -- Beachy, P A -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):255-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology and Genetics, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8824192" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; Cholesterol/*metabolism ; Dithiothreitol/pharmacology ; Drosophila ; *Drosophila Proteins ; *Embryonic Induction ; Embryonic and Fetal Development ; Hedgehog Proteins ; Humans ; Protein Processing, Post-Translational ; Proteins/genetics/*metabolism ; Signal Transduction ; *Trans-Activators
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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