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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: 2003-08-23
    Description: To elucidate gene function on a global scale, we identified pairs of genes that are coexpressed over 3182 DNA microarrays from humans, flies, worms, and yeast. We found 22,163 such coexpression relationships, each of which has been conserved across evolution. This conservation implies that the coexpression of these gene pairs confers a selective advantage and therefore that these genes are functionally related. Many of these relationships provide strong evidence for the involvement of new genes in core biological functions such as the cell cycle, secretion, and protein expression. We experimentally confirmed the predictions implied by some of these links and identified cell proliferation functions for several genes. By assembling these links into a gene-coexpression network, we found several components that were animal-specific as well as interrelationships between newly evolved and ancient modules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stuart, Joshua M -- Segal, Eran -- Koller, Daphne -- Kim, Stuart K -- New York, N.Y. -- Science. 2003 Oct 10;302(5643):249-55. Epub 2003 Aug 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford Medical Informatics, 251 Campus Drive, Medical School Office Building X-215, Stanford, CA 94305-5329, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12934013" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Caenorhabditis elegans/genetics ; Cell Cycle/genetics ; Cell Division/genetics ; Computational Biology ; Conserved Sequence ; Databases, Genetic ; Drosophila melanogaster/genetics ; *Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation ; Genes, Fungal ; Genes, Helminth ; Genes, Insect ; Humans ; Models, Statistical ; Mutation ; *Oligonucleotide Array Sequence Analysis ; Proteins/metabolism ; Saccharomyces cerevisiae/genetics ; Signal Transduction/genetics ; Species Specificity ; 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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  • 3
    Publication Date: 1998-08-14
    Description: The breast and ovarian cancer susceptibility gene BRCA1 encodes a zinc finger protein of unknown function. Association of the BRCA1 protein with the DNA repair protein Rad51 and changes in the phosphorylation and cellular localization of the protein after exposure to DNA-damaging agents are consistent with a role for BRCA1 in DNA repair. Here, it is shown that mouse embryonic stem cells deficient in BRCA1 are defective in the ability to carry out transcription-coupled repair of oxidative DNA damage, and are hypersensitive to ionizing radiation and hydrogen peroxide. These results suggest that BRCA1 participates, directly or indirectly, in transcription-coupled repair of oxidative DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gowen, L C -- Avrutskaya, A V -- Latour, A M -- Koller, B H -- Leadon, S A -- CA40453/CA/NCI NIH HHS/ -- CA70490/CA/NCI NIH HHS/ -- IP50CA58223/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 14;281(5379):1009-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Curriculum in Genetics and Molecular Biology and Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9703501" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; BRCA1 Protein/genetics/*physiology ; Cell Line ; DNA Damage ; *DNA Repair ; Hydrogen Peroxide ; Mice ; Oxidation-Reduction ; Stem Cells ; Thymine/analogs & derivatives/immunology/metabolism ; Transcription, Genetic ; Ultraviolet Rays
    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: 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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  • 5
    Publication Date: 2010-10-29
    Description: Biodiversity is rapidly declining, and this may negatively affect ecosystem processes, including economically important ecosystem services. Previous studies have shown that biodiversity has positive effects on organisms and processes across trophic levels. However, only a few studies have so far incorporated an explicit food-web perspective. In an eight-year biodiversity experiment, we studied an unprecedented range of above- and below-ground organisms and multitrophic interactions. A multitrophic data set originating from a single long-term experiment allows mechanistic insights that would not be gained from meta-analysis of different experiments. Here we show that plant diversity effects dampen with increasing trophic level and degree of omnivory. This was true both for abundance and species richness of organisms. Furthermore, we present comprehensive above-ground/below-ground biodiversity food webs. Both above ground and below ground, herbivores responded more strongly to changes in plant diversity than did carnivores or omnivores. Density and richness of carnivorous taxa was independent of vegetation structure. Below-ground responses to plant diversity were consistently weaker than above-ground responses. Responses to increasing plant diversity were generally positive, but were negative for biological invasion, pathogen infestation and hyperparasitism. Our results suggest that plant diversity has strong bottom-up effects on multitrophic interaction networks, with particularly strong effects on lower trophic levels. Effects on higher trophic levels are indirectly mediated through bottom-up trophic cascades.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scherber, Christoph -- Eisenhauer, Nico -- Weisser, Wolfgang W -- Schmid, Bernhard -- Voigt, Winfried -- Fischer, Markus -- Schulze, Ernst-Detlef -- Roscher, Christiane -- Weigelt, Alexandra -- Allan, Eric -- Bessler, Holger -- Bonkowski, Michael -- Buchmann, Nina -- Buscot, Francois -- Clement, Lars W -- Ebeling, Anne -- Engels, Christof -- Halle, Stefan -- Kertscher, Ilona -- Klein, Alexandra-Maria -- Koller, Robert -- Konig, Stephan -- Kowalski, Esther -- Kummer, Volker -- Kuu, Annely -- Lange, Markus -- Lauterbach, Dirk -- Middelhoff, Cornelius -- Migunova, Varvara D -- Milcu, Alexandru -- Muller, Ramona -- Partsch, Stephan -- Petermann, Jana S -- Renker, Carsten -- Rottstock, Tanja -- Sabais, Alexander -- Scheu, Stefan -- Schumacher, Jens -- Temperton, Vicky M -- Tscharntke, Teja -- England -- Nature. 2010 Nov 25;468(7323):553-6. doi: 10.1038/nature09492. Epub 2010 Oct 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Georg-August-University Gottingen, Department of Crop Sciences, Agroecology, Grisebachstrasse 6, 37077 Gottingen, Germany. christoph.scherber@agr.uni-goettingen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20981010" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; *Models, Biological ; *Plant Physiological Phenomena ; Population Density
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 1991-04-05
    Description: The natriuretic peptides are hormones that can stimulate natriuretic, diuretic, and vasorelaxant activity in vivo, presumably through the activation of two known cell surface receptor guanylyl cyclases (ANPR-A and ANPR-B). Although atrial natriuretic peptide (ANP) and, to a lesser extent, brain natriuretic peptide (BNP) are efficient activators of the ANPR-A guanylyl cyclase, neither hormone can significantly stimulate ANPR-B. A member of this hormone family, C-type natriuretic peptide (CNP), potently and selectively activated the human ANPR-B guanylyl cyclase. CNP does not increase guanosine 3',5'-monophosphate accumulation in cells expressing human ANPR-A. The affinity of CNP for ANPR-B is 50- or 500-fold higher than ANP or BNP, respectively. This ligand-receptor pair may be involved in the regulation of fluid homeostasis by the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koller, K J -- Lowe, D G -- Bennett, G L -- Minamino, N -- Kangawa, K -- Matsuo, H -- Goeddel, D V -- New York, N.Y. -- Science. 1991 Apr 5;252(5002):120-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Genentech, Inc., South San Francisco 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1672777" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atrial Natriuretic Factor/*physiology ; Cells, Cultured ; Cercopithecus aethiops ; Cloning, Molecular ; Dose-Response Relationship, Drug ; Guanylate Cyclase/metabolism ; Humans ; Natriuretic Peptide, Brain ; Natriuretic Peptide, C-Type ; Nerve Tissue Proteins/*pharmacology ; Receptors, Atrial Natriuretic Factor ; Receptors, Cell Surface/*physiology ; Recombinant Proteins ; Signal Transduction
    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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  • 7
    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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  • 8
    Publication Date: 1992-08-21
    Description: The cystic fibrosis transmembrane conductance regulator (CFTR) gene encodes an adenosine 3',5'-monophosphate (cyclic AMP)-activated chloride channel. In cystic fibrosis (CF) patients, loss of CFTR function because of a genetic mutation results in defective cyclic AMP-mediated chloride secretion across epithelia. Because of their potential role as an animal model for CF, mice with targeted disruption of the murine CFTR gene [CFTR(-/-)] were tested for abnormalities in epithelial chloride transport. In both freshly excised tissue from the intestine and in cultured epithelia from the proximal airways, the cyclic AMP-activated chloride secretory response was absent in CFTR(-/-) mice as compared to littermate controls. Thus, disruption of the murine CFTR gene results in the chloride transport abnormalities predicted from studies of human CF epithelia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clarke, L L -- Grubb, B R -- Gabriel, S E -- Smithies, O -- Koller, B H -- Boucher, R C -- GM20069/GM/NIGMS NIH HHS/ -- HL 42384/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1125-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of North Carolina, Chapel Hill 27514.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1380724" target="_blank"〉PubMed〈/a〉
    Keywords: Amiloride/pharmacology ; Animals ; Biological Transport ; Cells, Cultured ; Chlorides/*metabolism ; Colforsin/pharmacology ; Cyclic AMP/pharmacology ; Cystic Fibrosis/genetics/*metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator ; *Disease Models, Animal ; Epithelium/metabolism ; Intestines/metabolism ; Membrane Proteins/genetics/*physiology ; Mice ; Mutation ; Nose/metabolism ; Trachea/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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  • 9
    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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  • 10
    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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