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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-12-01
    Description: Prostaglandins and leukotrienes are potent eicosanoid lipid mediators derived from phospholipase-released arachidonic acid that are involved in numerous homeostatic biological functions and inflammation. They are generated by cyclooxygenase isozymes and 5-lipoxygenase, respectively, and their biosynthesis and actions are blocked by clinically relevant nonsteroidal anti-inflammatory drugs, the newer generation coxibs (selective inhibitors of cyclooxygenase-2), and leukotriene modifiers. The prime mode of prostaglandin and leukotriene action is through specific G protein-coupled receptors, many of which have been cloned recently, thus enabling specific receptor agonist and antagonist development. Important insights into the mechanisms of inflammatory responses, pain, and fever have been gleaned from our current understanding of eicosanoid biology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Funk, C D -- GM63130/GM/NIGMS NIH HHS/ -- HL53558/HL/NHLBI NIH HHS/ -- HL58464/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2001 Nov 30;294(5548):1871-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Experimental Therapeutics and Department of Pharmacology, University of Pennsylvania, Philadelphia, PA 19104, USA. colin@spirit.gcrc.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11729303" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology/therapeutic use ; Fever/drug therapy/metabolism ; Humans ; Inflammation/drug therapy/metabolism ; Leukotriene Antagonists ; Leukotrienes/agonists/biosynthesis/*metabolism ; Pain/drug therapy/metabolism ; Prostaglandin Antagonists/pharmacology/therapeutic use ; Prostaglandins/agonists/biosynthesis/*metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Leukotriene/metabolism ; Transcription Factors/metabolism
    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
    Publication Date: 2005-08-20
    Description: Several described growth factors influence the proliferation and regeneration of the intestinal epithelium. Using a transgenic mouse model, we identified a human gene, R-spondin1, with potent and specific proliferative effects on intestinal crypt cells. Human R-spondin1 (hRSpo1) is a thrombospondin domain-containing protein expressed in enteroendocrine cells as well as in epithelial cells in various tissues. Upon injection into mice, the protein induced rapid onset of crypt cell proliferation involving beta-catenin stabilization, possibly by a process that is distinct from the canonical Wnt-mediated signaling pathway. The protein also displayed efficacy in a model of chemotherapy-induced intestinal mucositis and may have therapeutic application in gastrointestinal diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Kyung-Ah -- Kakitani, Makoto -- Zhao, Jingsong -- Oshima, Takeshi -- Tang, Tom -- Binnerts, Minke -- Liu, Yi -- Boyle, Bryan -- Park, Emily -- Emtage, Peter -- Funk, Walter D -- Tomizuka, Kazuma -- New York, N.Y. -- Science. 2005 Aug 19;309(5738):1256-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nuvelo, Inc., 675 Almanor Avenue, Sunnyvale, CA 94085, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16109882" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/adverse effects ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Chimera ; Colon/cytology/pathology ; Cytoskeletal Proteins/metabolism ; Dose-Response Relationship, Drug ; Enteroendocrine Cells/metabolism ; Epithelial Cells/metabolism ; Fibroblast Growth Factor 7 ; Fibroblast Growth Factors/pharmacology ; Fluorouracil/adverse effects ; Glucagon-Like Peptides ; Humans ; Intestinal Mucosa/*cytology/metabolism/pathology ; Intestine, Small/cytology/pathology ; Mice ; Mice, Transgenic ; *Mitogens ; Neoplasm Transplantation ; Neoplasms, Experimental/drug therapy/pathology ; Peptides/pharmacology ; Proteins/pharmacology ; Recombinant Proteins/pharmacology ; Thrombospondins/genetics/metabolism/pharmacology/*physiology ; Tongue/drug effects/pathology ; Trans-Activators/metabolism ; Wnt Proteins ; Wnt3 Protein ; beta Catenin
    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
    Publication Date: 1995-09-01
    Description: Eukaryotic chromosomes are capped with repetitive telomere sequences that protect the ends from damage and rearrangements. Telomere repeats are synthesized by telomerase, a ribonucleic acid (RNA)-protein complex. Here, the cloning of the RNA component of human telomerase, termed hTR, is described. The template region of hTR encompasses 11 nucleotides (5'-CUAACCCUAAC) complementary to the human telomere sequence (TTAGGG)n. Germline tissues and tumor cell lines expressed more hTR than normal somatic cells and tissues, which have no detectable telomerase activity. Human cell lines that expressed hTR mutated in the template region generated the predicted mutant telomerase activity. HeLa cells transfected with an antisense hTR lost telomeric DNA and began to die after 23 to 26 doublings. Thus, human telomerase is a critical enzyme for the long-term proliferation of immortal tumor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, J -- Funk, W D -- Wang, S S -- Weinrich, S L -- Avilion, A A -- Chiu, C P -- Adams, R R -- Chang, E -- Allsopp, R C -- Yu, J -- AG09383/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1995 Sep 1;269(5228):1236-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geron Corporation, Menlo Park, CA 94025, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7544491" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Death ; *Cell Division ; Cell Line ; Cloning, Molecular ; DNA Nucleotidylexotransferase/antagonists & ; inhibitors/chemistry/genetics/*metabolism ; HeLa Cells ; Humans ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Polymerase Chain Reaction ; RNA/chemistry/genetics/*metabolism ; Templates, Genetic ; Transfection ; Tumor Cells, Cultured
    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
    Publication Date: 1995-09-01
    Description: Telomerase synthesizes telomeric DNA repeats onto chromosome ends de novo. The mouse telomerase RNA component was cloned and contained only 65 percent sequence identity with the human telomerase RNA. Alteration of the template region in vivo generated altered telomerase products. The shorter template regions of the mouse and other rodent telomerase RNAs could account for the shorter distribution of products (processivity) generated by the mouse enzyme relative to the human telomerase. Amounts of telomerase RNA increased in immortal cells derived from primary mouse fibroblasts. RNA was detected in all newborn mouse tissues tested but was decreased during postnatal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blasco, M A -- Funk, W -- Villeponteau, B -- Greider, C W -- AG09383/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1995 Sep 1;269(5228):1267-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7544492" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Animals, Newborn ; Base Sequence ; Brain/enzymology ; Cell Line, Transformed ; Cloning, Molecular ; DNA Nucleotidylexotransferase/antagonists & ; inhibitors/chemistry/genetics/*metabolism ; *Gene Expression Regulation, Developmental ; Humans ; Kidney/enzymology ; Liver/enzymology ; Mice ; Molecular Sequence Data ; Muridae ; Mutagenesis ; Oligonucleotides, Antisense/pharmacology ; RNA/chemistry/genetics/*metabolism ; Templates, Genetic ; 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
    Publication Date: 2015-03-15
    Description: Despite some notable successes in the control of infectious diseases, transmissible pathogens still pose an enormous threat to human and animal health. The ecological and evolutionary dynamics of infections play out on a wide range of interconnected temporal, organizational, and spatial scales, which span hours to months, cells to ecosystems, and local to global spread. Moreover, some pathogens are directly transmitted between individuals of a single species, whereas others circulate among multiple hosts, need arthropod vectors, or can survive in environmental reservoirs. Many factors, including increasing antimicrobial resistance, increased human connectivity and changeable human behavior, elevate prevention and control from matters of national policy to international challenge. In the face of this complexity, mathematical models offer valuable tools for synthesizing information to understand epidemiological patterns, and for developing quantitative evidence for decision-making in global health.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445966/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445966/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heesterbeek, Hans -- Anderson, Roy M -- Andreasen, Viggo -- Bansal, Shweta -- De Angelis, Daniela -- Dye, Chris -- Eames, Ken T D -- Edmunds, W John -- Frost, Simon D W -- Funk, Sebastian -- Hollingsworth, T Deirdre -- House, Thomas -- Isham, Valerie -- Klepac, Petra -- Lessler, Justin -- Lloyd-Smith, James O -- Metcalf, C Jessica E -- Mollison, Denis -- Pellis, Lorenzo -- Pulliam, Juliet R C -- Roberts, Mick G -- Viboud, Cecile -- Isaac Newton Institute IDD Collaboration -- U01 GM110721/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 Mar 13;347(6227):aaa4339. doi: 10.1126/science.aaa4339.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Faculty of Veterinary Medicine, University of Utrecht, Utrecht, Netherlands. j.a.p.heesterbeek@uu.nl. ; School of Public Health, Imperial College, London, UK. ; Roskilde University, Roskilde, Denmark. ; Georgetown University, Washington, DC, USA. ; MRC Biostatistics Unit, Cambridge, UK. ; WHO, Geneva, Switzerland. ; Centre for the Mathematical Modelling of Infectious Diseases, London School of Hygiene Tropical Medicine, London, UK. ; University of Cambridge, Cambridge, UK. ; School of Life Sciences, University of Warwick, UK. School of Tropical Medicine, University of Liverpool, UK. ; Warwick Mathematics Institute, University of Warwick, Coventry, UK. ; Department of Statistical Science, University College London, London, UK. ; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. ; Department of Ecology and Evolutionary Biology, University of California, Los Angeles, CA, USA. ; Department of Zoology, University of Oxford, Oxford, UK, and Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ, USA. ; Heriot-Watt University, Edinburgh, UK. ; Department of Biology-Emerging Pathogens Institute, University of Florida, Gainesville, FL, USA. Division of International Epidemiology and Population Studies, Fogarty International Center, NIH, Bethesda, MD, USA. ; Institute of Natural and Mathematical Sciences, Massey University, Auckland, New Zealand. ; Division of International Epidemiology and Population Studies, Fogarty International Center, NIH, Bethesda, MD, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25766240" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Reproduction Number ; Coinfection ; Communicable Disease Control ; *Communicable Diseases/epidemiology/transmission ; Communicable Diseases, Emerging/epidemiology/transmission ; Disease Outbreaks ; *Global Health ; Health Policy ; Hemorrhagic Fever, Ebola/epidemiology ; Humans ; *Models, Biological ; *Public Health ; Zoonoses/epidemiology/transmission
    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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