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  • 1
    Electronic Resource
    Electronic Resource
    Weinheim : Wiley-Blackwell
    Journal of High Resolution Chromatography 7 (1984), S. 43-43 
    ISSN: 0935-6304
    Keywords: GC/MS ; Coupling a GC to a GC/MS-System ; Chemistry ; Analytical Chemistry and Spectroscopy
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
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  • 2
    Publication Date: 2002-04-20
    Description: Thromboxane (Tx) A2 is a vasoconstrictor and platelet agonist. Aspirin affords cardioprotection through inhibition of TxA2 formation by platelet cyclooxygenase (COX-1). Prostacyclin (PGI2) is a vasodilator that inhibits platelet function. Here we show that injury-induced vascular proliferation and platelet activation are enhanced in mice that are genetically deficient in the PGI2 receptor (IP) but are depressed in mice genetically deficient in the TxA2 receptor (TP) or treated with a TP antagonist. The augmented response to vascular injury was abolished in mice deficient in both receptors. Thus, PGI2 modulates platelet-vascular interactions in vivo and specifically limits the response to TxA2. This interplay may help explain the adverse cardiovascular effects associated with selective COX-2 inhibitors, which, unlike aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs), inhibit PGI2 but not TxA2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, Yan -- Austin, Sandra C -- Rocca, Bianca -- Koller, Beverly H -- Coffman, Thomas M -- Grosser, Tilo -- Lawson, John A -- FitzGerald, Garret A -- HL 54500/HL/NHLBI NIH HHS/ -- HL 62250/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2002 Apr 19;296(5567):539-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Experimental Therapeutics, 153 Johnson Pavilion, 3620 Hamilton Walk, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6084, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11964481" target="_blank"〉PubMed〈/a〉
    Keywords: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid/pharmacology ; Animals ; *Carotid Artery Injuries/pathology ; Carotid Artery, Common/cytology/drug effects/physiology ; Cell Division ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors/adverse effects/therapeutic use ; Endothelium, Vascular/cytology/drug effects/*physiology ; Epoprostenol/metabolism/*physiology ; Humans ; Isoenzymes/antagonists & inhibitors ; Lactones/adverse effects/therapeutic use ; Male ; Membrane Proteins ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Muscle, Smooth, Vascular/cytology/drug effects/physiology ; Naphthalenes ; *Platelet Activation/drug effects ; Platelet Aggregation/drug effects ; Propionates ; Prostaglandin-Endoperoxide Synthases ; Receptors, Epoprostenol ; Receptors, Prostaglandin/physiology ; Receptors, Thromboxane/antagonists & inhibitors/genetics/physiology ; Sulfones ; Tetrahydronaphthalenes/pharmacology ; Thromboxane A2/*physiology ; Tunica Intima/cytology
    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: 1992-08-21
    Description: Cystic fibrosis results from defects in the gene encoding a cyclic adenosine monophosphate-dependent chloride ion channel known as the cystic fibrosis transmembrane conductance regulator (CFTR). To create an animal model for cystic fibrosis, mice were generated from embryonic stem cells in which the CFTR gene was disrupted by gene targeting. Mice homozygous for the disrupted gene display many features common to young human cystic fibrosis patients, including failure to thrive, meconium ileus, alteration of mucous and serous glands, and obstruction of glandlike structures with inspissated eosinophilic material. Death resulting from intestinal obstruction usually occurs before 40 days of age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snouwaert, J N -- Brigman, K K -- Latour, A M -- Malouf, N N -- Boucher, R C -- Smithies, O -- Koller, B H -- GM20069/GM/NIGMS NIH HHS/ -- HL 42384/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1083-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of North Carolina, Chapel Hill 27599-7020.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1380723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cystic Fibrosis/*genetics/pathology/physiopathology ; Cystic Fibrosis Transmembrane Conductance Regulator ; Digestive System/metabolism/pathology ; *Disease Models, Animal ; Exocrine Glands/pathology ; Gallbladder/pathology ; Genitalia, Male/pathology ; Genotype ; Growth ; Intestinal Obstruction/etiology/pathology ; Liver/pathology ; Male ; Meconium/metabolism ; Membrane Proteins/*genetics ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mucus/metabolism ; Mutagenesis ; Pancreas/pathology ; RNA, Messenger/metabolism ; Salivary Glands/pathology
    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: 1990-06-08
    Description: Major histocompatibility class I proteins display viral and self antigens to potentially responsive cells and are important for the maturation of T cells; beta 2-microglobulin (beta 2M) is required for their normal expression. Mouse chimeras derived from embryonic stem cells with a disrupted beta 2M gene transmitted the inactivated gene to their progeny. Animals homozygous for the mutated beta 2M gene were obtained at expected frequencies after further breeding. The homozygotes appeared normal, although no class I antigens could be detected on their cells and the animals are grossly deficient in CD4- CD8+ T cells, which normally mediate cytotoxic T cell function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koller, B H -- Marrack, P -- Kappler, J W -- Smithies, O -- AI-18785/AI/NIAID NIH HHS/ -- GM20069/GM/NIGMS NIH HHS/ -- HL37001/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Jun 8;248(4960):1227-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of North Carolina, Chapel Hill 27599-7525.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2112266" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/*genetics ; Chimera ; Gene Expression ; Genes ; Genes, MHC Class I ; Histocompatibility Antigens Class I/*genetics ; Lymph Nodes/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; *Mutation ; Spleen/immunology ; T-Lymphocytes/*immunology ; beta 2-Microglobulin/*deficiency/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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  • 5
    Publication Date: 2004-11-20
    Description: Female gender affords relative protection from cardiovascular disease until the menopause. We report that estrogen acts on estrogen receptor subtype alpha to up-regulate the production of atheroprotective prostacyclin, PGI2, by activation of cyclooxygenase 2 (COX-2). This mechanism restrained both oxidant stress and platelet activation that contribute to atherogenesis in female mice. Deletion of the PGI2 receptor removed the atheroprotective effect of estrogen in ovariectomized female mice. This suggests that chronic treatment of patients with selective inhibitors of COX-2 could undermine protection from cardiovascular disease in premenopausal females.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, Karine M -- Lawson, John A -- Fries, Susanne -- Koller, Beverley -- Rader, Daniel J -- Smyth, Emer M -- Fitzgerald, Garret A -- HL62250/HL/NHLBI NIH HHS/ -- HL70128/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 10;306(5703):1954-7. Epub 2004 Nov 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Translational Medicine and Therapeutics, University of Pennsylvania, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15550624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antioxidants/metabolism ; Arteriosclerosis/metabolism/pathology/*prevention & control ; Cardiovascular Diseases/chemically induced ; Cells, Cultured ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors/adverse effects/pharmacology ; Epoprostenol/biosynthesis/metabolism/*physiology ; Estradiol/pharmacology ; Estrogen Receptor alpha/metabolism ; Female ; Hydrogen Peroxide/pharmacology ; Isoenzymes/*metabolism ; Lactones/adverse effects/pharmacology ; Lipid Peroxidation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular/drug effects/metabolism ; Myocytes, Smooth Muscle/cytology/drug effects/metabolism ; Ovariectomy ; Oxidative Stress ; Platelet Activation ; Prostaglandin-Endoperoxide Synthases/*metabolism ; Receptors, Epoprostenol/genetics/physiology ; Receptors, LDL/genetics/physiology ; Sex Characteristics ; Sulfones/adverse effects/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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  • 6
    Publication Date: 1992-03-20
    Description: Intracranial infection of normal mice with lymphocytic choriomeningitis virus (LCMV) causes meningitis and death mediated by CD8+ major histocompatibility complex (MHC) class I-restricted cytotoxic T lymphocytes (CTLs). beta 2-Microglobulin-deficient mice (beta 2M-/-) do not express functional MHC class I proteins and do not produce significant numbers of CD8+ T cells. When beta 2M-/- mice were infected with LCMV, many died from LCMV disease and produced a specific response to LCMV mediated by CD4+ CTLs that were class II-restricted. In these mice, CD4+ CTLs may compensate for the lack of CD8+ CTLs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, D -- Koller, B H -- Whitton, J L -- LaPan, K E -- Brigman, K K -- Frelinger, J A -- AI-20288/AI/NIAID NIH HHS/ -- AI-29324/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Mar 20;255(5051):1576-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of North Carolina, Chapel Hill 27599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1347959" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD8/immunology ; CD4-Positive T-Lymphocytes/immunology ; Cytotoxicity, Immunologic ; H-2 Antigens/immunology ; Histocompatibility Antigens Class II/*immunology ; Lymphocyte Depletion ; Lymphocytic Choriomeningitis/*immunology ; Lymphocytic choriomeningitis virus ; Mice ; Mice, Inbred C57BL ; Spleen/immunology ; T-Lymphocytes, Cytotoxic/*immunology ; beta 2-Microglobulin/*deficiency
    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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