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  • 1
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    Oxidative damage linked to neurodegeneration by selective alpha-synuclein nitration in synucleinopathy lesions (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-04
    Description: Aggregated alpha-synuclein proteins form brain lesions that are hallmarks of neurodegenerative synucleinopathies, and oxidative stress has been implicated in the pathogenesis of some of these disorders. Using antibodies to specific nitrated tyrosine residues in alpha-synuclein, we demonstrate extensive and widespread accumulations of nitrated alpha-synuclein in the signature inclusions of Parkinson's disease, dementia with Lewy bodies, the Lewy body variant of Alzheimer's disease, and multiple system atrophy brains. We also show that nitrated alpha-synuclein is present in the major filamentous building blocks of these inclusions, as well as in the insoluble fractions of affected brain regions of synucleinopathies. The selective and specific nitration of alpha-synuclein in these disorders provides evidence to directly link oxidative and nitrative damage to the onset and progression of neurodegenerative synucleinopathies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giasson, B I -- Duda, J E -- Murray, I V -- Chen, Q -- Souza, J M -- Hurtig, H I -- Ischiropoulos, H -- Trojanowski, J Q -- Lee, V M -- New York, N.Y. -- Science. 2000 Nov 3;290(5493):985-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurodegenerative Disease Research and Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11062131" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism/pathology ; Antibodies, Monoclonal ; Blotting, Western ; Brain/*metabolism/pathology ; Brain Chemistry ; Enzyme-Linked Immunosorbent Assay ; Fluorescent Antibody Technique ; Humans ; Immunohistochemistry ; Lewy Bodies/chemistry ; Lewy Body Disease/metabolism/pathology ; Microscopy, Immunoelectron ; Multiple System Atrophy/metabolism/pathology ; Nerve Tissue Proteins/analysis/immunology/*metabolism ; Neurodegenerative Diseases/*metabolism/*pathology ; Neurons/chemistry/metabolism/ultrastructure ; *Oxidative Stress ; Parkinson Disease/metabolism/pathology ; Synucleins ; Tyrosine/*analogs & derivatives/analysis/immunology/*metabolism ; alpha-Synuclein
    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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    Detection of cell-affecting agents with a silicon biosensor (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-10-13
    Description: Cellular metabolism is affected by many factors in a cell's environment. Given a sufficiently sensitive method for measuring cellular metabolic rates, it should be possible to detect a wide variety of chemical and physical stimuli. A biosensor has been constructed in which living cells are confined to a flow chamber in which a potentiometric sensor continually measures the rate of production of acidic metabolites. Exploratory studies demonstrate several applications of the device in basic science and technology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parce, J W -- Owicki, J C -- Kercso, K M -- Sigal, G B -- Wada, H G -- Muir, V C -- Bousse, L J -- Ross, K L -- Sikic, B I -- McConnell, H M -- R01-CA-4217/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1989 Oct 13;246(4927):243-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Devices Corporation, Menlo Park, CA 94025.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2799384" target="_blank"〉PubMed〈/a〉
    Keywords: *Biosensing Techniques ; Carbonyl Cyanide m-Chlorophenyl Hydrazone/pharmacology ; Cells/*metabolism ; Cells, Cultured/drug effects/metabolism ; Epidermal Growth Factor/pharmacology ; Flow Cytometry ; Humans ; Oxygen Consumption ; Silicon
    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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    Neuroscience. What are mini-brains? (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bae, Byoung-il -- Walsh, Christopher A -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Oct 11;342(6155):200-1. doi: 10.1126/science.1245812.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics and Genomics, Manton Center for Orphan Disease, and Howard Hughes Medical Institute, Children's Hospital Boston, Department of Neurology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24115427" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*growth & development/*pathology ; Humans ; Microcephaly/*pathology ; *Models, Biological ; Organoids/*cytology/*growth & development ; Tissue Culture Techniques/*methods
    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
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    Evolutionarily dynamic alternative splicing of GPR56 regulates regional cerebral cortical patterning (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-02-18
    Description: The human neocortex has numerous specialized functional areas whose formation is poorly understood. Here, we describe a 15-base pair deletion mutation in a regulatory element of GPR56 that selectively disrupts human cortex surrounding the Sylvian fissure bilaterally including "Broca's area," the primary language area, by disrupting regional GPR56 expression and blocking RFX transcription factor binding. GPR56 encodes a heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptor required for normal cortical development and is expressed in cortical progenitor cells. GPR56 expression levels regulate progenitor proliferation. GPR56 splice forms are highly variable between mice and humans, and the regulatory element of gyrencephalic mammals directs restricted lateral cortical expression. Our data reveal a mechanism by which control of GPR56 expression pattern by multiple alternative promoters can influence stem cell proliferation, gyral patterning, and, potentially, neocortex evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4480613/" 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/PMC4480613/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bae, Byoung-Il -- Tietjen, Ian -- Atabay, Kutay D -- Evrony, Gilad D -- Johnson, Matthew B -- Asare, Ebenezer -- Wang, Peter P -- Murayama, Ayako Y -- Im, Kiho -- Lisgo, Steven N -- Overman, Lynne -- Sestan, Nenad -- Chang, Bernard S -- Barkovich, A James -- Grant, P Ellen -- Topcu, Meral -- Politsky, Jeffrey -- Okano, Hideyuki -- Piao, Xianhua -- Walsh, Christopher A -- 2R01NS035129/NS/NINDS NIH HHS/ -- G0700089/Medical Research Council/United Kingdom -- GR082557/Wellcome Trust/United Kingdom -- HHSN275200900011C/PHS HHS/ -- N01-HD-9-0011/HD/NICHD NIH HHS/ -- R01 NS035129/NS/NINDS NIH HHS/ -- U01 MH081896/MH/NIMH NIH HHS/ -- U01MH081896/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Feb 14;343(6172):764-8. doi: 10.1126/science.1244392.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics and Genomics, Manton Center for Orphan Disease, and Howard Hughes Medical Institute, Boston Children's Hospital, Broad Institute of MIT and Harvard, and Departments of Pediatrics and Neurology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24531968" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Animals ; Base Sequence ; Biological Evolution ; Body Patterning/*genetics ; Cats ; Cell Proliferation ; Cerebral Cortex/anatomy & histology/cytology/*embryology ; Codon, Nonsense ; Frontal Lobe/anatomy & histology/cytology/embryology ; Genetic Variation ; Haplotypes ; Humans ; Mice ; Molecular Sequence Data ; Neural Stem Cells/cytology/*physiology ; Pedigree ; Promoter Regions, Genetic/genetics ; Receptors, G-Protein-Coupled/*genetics ; Sequence Deletion
    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-specific functional impairments in distinct tau isoforms of hereditary FTDP-17 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-04
    Description: Tau proteins aggregate as cytoplasmic inclusions in a number of neurodegenerative diseases, including Alzheimer's disease and hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). Over 10 exonic and intronic mutations in the tau gene have been identified in about 20 FTDP-17 families. Analyses of soluble and insoluble tau proteins from brains of FTDP-17 patients indicated that different pathogenic mutations differentially altered distinct biochemical properties and stoichiometry of brain tau isoforms. Functional assays of recombinant tau proteins with different FTDP-17 missense mutations implicated all but one of these mutations in disease pathogenesis by reducing the ability of tau to bind microtubules and promote microtubule assembly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hong, M -- Zhukareva, V -- Vogelsberg-Ragaglia, V -- Wszolek, Z -- Reed, L -- Miller, B I -- Geschwind, D H -- Bird, T D -- McKeel, D -- Goate, A -- Morris, J C -- Wilhelmsen, K C -- Schellenberg, G D -- Trojanowski, J Q -- Lee, V M -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1914-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9836646" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Brain/*metabolism ; Cerebellum/metabolism ; Chromosomes, Human, Pair 17 ; Dementia/*genetics/metabolism ; Frontal Lobe/metabolism ; Humans ; Microtubules/*metabolism ; Mutation ; Mutation, Missense ; Parkinson Disease, Secondary/*genetics/metabolism ; Phosphorylation ; Protein Isoforms/chemistry/genetics/metabolism ; Recombinant Proteins/metabolism ; Solubility ; Syndrome ; tau Proteins/chemistry/*genetics/*metabolism
    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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    The influence of CCL3L1 gene-containing segmental duplications on HIV-1/AIDS susceptibility (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-08
    Description: Segmental duplications in the human genome are selectively enriched for genes involved in immunity, although the phenotypic consequences for host defense are unknown. We show that there are significant interindividual and interpopulation differences in the copy number of a segmental duplication encompassing the gene encoding CCL3L1 (MIP-1alphaP), a potent human immunodeficiency virus-1 (HIV-1)-suppressive chemokine and ligand for the HIV coreceptor CCR5. Possession of a CCL3L1 copy number lower than the population average is associated with markedly enhanced HIV/acquired immunodeficiency syndrome (AIDS) susceptibility. This susceptibility is even greater in individuals who also possess disease-accelerating CCR5 genotypes. This relationship between CCL3L1 dose and altered HIV/AIDS susceptibility points to a central role for CCL3L1 in HIV/AIDS pathogenesis and indicates that differences in the dose of immune response genes may constitute a genetic basis for variable responses to infectious diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gonzalez, Enrique -- Kulkarni, Hemant -- Bolivar, Hector -- Mangano, Andrea -- Sanchez, Racquel -- Catano, Gabriel -- Nibbs, Robert J -- Freedman, Barry I -- Quinones, Marlon P -- Bamshad, Michael J -- Murthy, Krishna K -- Rovin, Brad H -- Bradley, William -- Clark, Robert A -- Anderson, Stephanie A -- O'connell, Robert J -- Agan, Brian K -- Ahuja, Seema S -- Bologna, Rosa -- Sen, Luisa -- Dolan, Matthew J -- Ahuja, Sunil K -- AI043279/AI/NIAID NIH HHS/ -- AI046326/AI/NIAID NIH HHS/ -- MH069270/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 4;307(5714):1434-40. Epub 2005 Jan 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Veterans Administration Research Center for AIDS and HIV-1 Infection, South Texas Veterans Health Care System, and Department of Medicine, University of Texas Health Science Center, San Antonio, TX 78229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15637236" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Animals ; Chemokines, CC/*genetics/metabolism ; Child ; Cohort Studies ; Continental Population Groups/genetics ; Disease Progression ; Ethnic Groups/genetics ; Female ; *Gene Dosage ; *Gene Duplication ; *Genetic Predisposition to Disease ; Genotype ; HIV Infections/epidemiology/*genetics/*immunology/virology ; *HIV-1/metabolism ; Humans ; Male ; Middle Aged ; Pan troglodytes/genetics ; Phenotype ; Public Health ; Receptors, CCR5/genetics/metabolism ; Selection, Genetic
    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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  • 7
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    Initiation and synergistic fibrillization of tau and alpha-synuclein (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-26
    Description: Alpha-synuclein (alpha-syn) and tau polymerize into amyloid fibrils and form intraneuronal filamentous inclusions characteristic of neurodegenerative diseases. We demonstrate that alpha-syn induces fibrillization of tau and that coincubation of tau and alpha-syn synergistically promotes fibrillization of both proteins. The in vivo relevance of these findings is grounded in the co-occurrence of alpha-syn and tau filamentous amyloid inclusions in humans, in single transgenic mice that express A53T human alpha-syn in neurons, and in oligodendrocytes of bigenic mice that express wild-type human alpha-syn plus P301L mutant tau. This suggests that interactions between alpha-syn and tau can promote their fibrillization and drive the formation of pathological inclusions in human neurodegenerative diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giasson, Benoit I -- Forman, Mark S -- Higuchi, Makoto -- Golbe, Lawrence I -- Graves, Charles L -- Kotzbauer, Paul T -- Trojanowski, John Q -- Lee, Virginia M-Y -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):636-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12714745" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/chemistry/metabolism ; Animals ; Biopolymers ; *Brain Chemistry ; Humans ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Transgenic ; Microscopy, Electron ; Microscopy, Fluorescence ; Microscopy, Immunoelectron ; Nerve Tissue Proteins/analysis/*chemistry/metabolism ; Neurodegenerative Diseases/metabolism ; Neurons/chemistry ; Oligodendroglia/chemistry ; Protein Conformation ; Protein Isoforms/chemistry/metabolism ; Synucleins ; Tauopathies/metabolism ; alpha-Synuclein ; tau Proteins/analysis/*chemistry/metabolism
    Print ISSN: 0036-8075
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  • 8
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    Inactivation of TNF signaling by rationally designed dominant-negative TNF variants (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: Tumor necrosis factor (TNF) is a key regulator of inflammatory responses and has been implicated in many pathological conditions. We used structure-based design to engineer variant TNF proteins that rapidly form heterotrimers with native TNF to give complexes that neither bind to nor stimulate signaling through TNF receptors. Thus, TNF is inactivated by sequestration. Dominant-negative TNFs represent a possible approach to anti-inflammatory biotherapeutics, and experiments in animal models show that the strategy can attenuate TNF-mediated pathology. Similar rational design could be used to engineer inhibitors of additional TNF superfamily cytokines as well as other multimeric ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steed, Paul M -- Tansey, Malu G -- Zalevsky, Jonathan -- Zhukovsky, Eugene A -- Desjarlais, John R -- Szymkowski, David E -- Abbott, Christina -- Carmichael, David -- Chan, Cheryl -- Cherry, Lisa -- Cheung, Peter -- Chirino, Arthur J -- Chung, Hyo H -- Doberstein, Stephen K -- Eivazi, Araz -- Filikov, Anton V -- Gao, Sarah X -- Hubert, Rene S -- Hwang, Marian -- Hyun, Linus -- Kashi, Sandhya -- Kim, Alice -- Kim, Esther -- Kung, James -- Martinez, Sabrina P -- Muchhal, Umesh S -- Nguyen, Duc-Hanh T -- O'Brien, Christopher -- O'Keefe, Donald -- Singer, Karen -- Vafa, Omid -- Vielmetter, Jost -- Yoder, Sean C -- Dahiyat, Bassil I -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1895-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Xencor, 111 West Lemon Avenue, Monrovia, CA 91016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512626" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Antigens, CD/metabolism ; Apoptosis ; Arthritis, Experimental/drug therapy ; Biopolymers ; Caspases/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Computer Simulation ; Disease Progression ; Enzyme-Linked Immunosorbent Assay ; Female ; Galactosamine/pharmacology ; HeLa Cells ; Humans ; Liver/drug effects ; NF-kappa B/metabolism ; Point Mutation ; *Protein Engineering ; Rats ; Receptors, Tumor Necrosis Factor/metabolism ; Receptors, Tumor Necrosis Factor, Type I ; Receptors, Tumor Necrosis Factor, Type II ; *Signal Transduction ; Transcription Factor RelA ; Transcription, Genetic ; Tumor Necrosis Factor-alpha/*antagonists & ; inhibitors/genetics/metabolism/*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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  • 9
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    A potential noninvasive neurobiological test for Alzheimer's disease (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: Currently Alzheimer's disease, which affects more than 20 million people worldwide, can only be definitely diagnosed by histological examination of brain tissue obtained at autopsy or biopsy. There is a great need for an early, noninvasive, sensitive, and easily administered diagnostic test of Alzheimer's disease. Here it is reported that patients diagnosed with probable Alzheimer's disease by standard clinical criteria exhibited a marked hypersensitivity in their pupil dilation response to a cholinergic antagonist, tropicamide, placed in their eyes. It was possible to distinguish 18 of 19 individuals (95%) either clinically diagnosed with Alzheimer's disease or classified as suspect Alzheimer's individuals by neuropsychological screening from 30 of 32 normal elderly controls (94%).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scinto, L F -- Daffner, K R -- Dressler, D -- Ransil, B I -- Rentz, D -- Weintraub, S -- Mesulam, M -- Potter, H -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1051-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Eye Movements and Higher Cortical Functions, Brigham and Women's Hospital, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973660" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Alzheimer Disease/*diagnosis/physiopathology ; Dementia/physiopathology ; Female ; Humans ; Male ; Neuropsychological Tests ; Pupil/*drug effects ; Reproducibility of Results ; Sensitivity and Specificity ; *Tropicamide/pharmacology
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    The challenge of micropollutants in aquatic systems (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-26
    Description: The increasing worldwide contamination of freshwater systems with thousands of industrial and natural chemical compounds is one of the key environmental problems facing humanity. Although most of these compounds are present at low concentrations, many of them raise considerable toxicological concerns, particularly when present as components of complex mixtures. Here we review three scientific challenges in addressing water-quality problems caused by such micropollutants. First, tools to assess the impact of these pollutants on aquatic life and human health must be further developed and refined. Second, cost-effective and appropriate remediation and water-treatment technologies must be explored and implemented. Third, usage and disposal strategies, coupled with the search for environmentally more benign products and processes, should aim to minimize introduction of critical pollutants into the aquatic environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwarzenbach, Rene P -- Escher, Beate I -- Fenner, Kathrin -- Hofstetter, Thomas B -- Johnson, C Annette -- von Gunten, Urs -- Wehrli, Bernhard -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1072-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eawag, Swiss Federal Institute of Aquatic Science and Technology, 8600 Dubendorf, Switzerland. rene.schwarzenbach@env.ethz.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931750" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodegradation, Environmental ; Complex Mixtures/analysis/toxicity ; Developing Countries ; Ecosystem ; Environment ; *Fresh Water ; Humans ; Risk Assessment ; Toxicity Tests ; *Water Pollutants, Chemical/analysis/classification/metabolism/toxicity ; *Water Pollution/prevention & control ; *Water Purification/methods ; Water Supply
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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