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  • Male  (44)
  • 2005-2009  (30)
  • 2000-2004  (14)
  • 11
    Publikationsdatum: 2008-01-26
    Beschreibung: The hippocampus is an area of the brain involved in learning and memory. It contains parallel excitatory pathways referred to as the trisynaptic pathway (which carries information as follows: entorhinal cortex --〉 dentate gyrus --〉 CA3 --〉 CA1 --〉 entorhinal cortex) and the monosynaptic pathway (entorhinal cortex --〉 CA1 --〉 entorhinal cortex). We developed a generally applicable tetanus toxin-based method for transgenic mice that permits inducible and reversible inhibition of synaptic transmission and applied it to the trisynaptic pathway while preserving transmission in the monosynaptic pathway. We found that synaptic output from CA3 in the trisynaptic pathway is dispensable and the short monosynaptic pathway is sufficient for incremental spatial learning. In contrast, the full trisynaptic pathway containing CA3 is required for rapid one-trial contextual learning, for pattern completion-based memory recall, and for spatial tuning of CA1 cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakashiba, Toshiaki -- Young, Jennie Z -- McHugh, Thomas J -- Buhl, Derek L -- Tonegawa, Susumu -- P50-MH58880/MH/NIMH NIH HHS/ -- R01-MH078821/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2008 Feb 29;319(5867):1260-4. doi: 10.1126/science.1151120. Epub 2008 Jan 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Picower Institute for Learning and Memory, Howard Hughes Medical Institute, RIKEN-MIT Neuroscience Research Center, Department of Biology and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18218862" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Action Potentials ; Animals ; Crosses, Genetic ; Dentate Gyrus/physiology ; Electrophysiology ; Entorhinal Cortex/physiology ; Excitatory Postsynaptic Potentials ; Female ; Hippocampus/*physiology ; Interneurons/physiology ; Male ; *Maze Learning ; Mental Recall ; Metalloendopeptidases/genetics ; Mice ; Mice, Transgenic ; Neural Pathways ; Pyramidal Cells/*physiology ; *Synaptic Transmission ; Tetanus Toxin/genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 12
    Publikationsdatum: 2009-03-03
    Beschreibung: Amyotrophic lateral sclerosis (ALS) is a fatal degenerative motor neuron disorder. Ten percent of cases are inherited; most involve unidentified genes. We report here 13 mutations in the fused in sarcoma/translated in liposarcoma (FUS/TLS) gene on chromosome 16 that were specific for familial ALS. The FUS/TLS protein binds to RNA, functions in diverse processes, and is normally located predominantly in the nucleus. In contrast, the mutant forms of FUS/TLS accumulated in the cytoplasm of neurons, a pathology that is similar to that of the gene TAR DNA-binding protein 43 (TDP43), whose mutations also cause ALS. Neuronal cytoplasmic protein aggregation and defective RNA metabolism thus appear to be common pathogenic mechanisms involved in ALS and possibly in other neurodegenerative disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kwiatkowski, T J Jr -- Bosco, D A -- Leclerc, A L -- Tamrazian, E -- Vanderburg, C R -- Russ, C -- Davis, A -- Gilchrist, J -- Kasarskis, E J -- Munsat, T -- Valdmanis, P -- Rouleau, G A -- Hosler, B A -- Cortelli, P -- de Jong, P J -- Yoshinaga, Y -- Haines, J L -- Pericak-Vance, M A -- Yan, J -- Ticozzi, N -- Siddique, T -- McKenna-Yasek, D -- Sapp, P C -- Horvitz, H R -- Landers, J E -- Brown, R H Jr -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1205-8. doi: 10.1126/science.1166066.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA. tkwiatkowski@partners.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19251627" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Age of Onset ; Amino Acid Substitution ; Amyotrophic Lateral Sclerosis/*genetics/metabolism/pathology ; Animals ; Brain/pathology ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Chromosomes, Human, Pair 16/*genetics ; Cytoplasm/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Exons ; Female ; Humans ; Male ; Mice ; Motor Neurons/chemistry/metabolism/ultrastructure ; Mutant Proteins/chemistry/genetics/metabolism ; *Mutation, Missense ; Neurons/metabolism/ultrastructure ; RNA/metabolism ; RNA-Binding Protein FUS/chemistry/*genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Analysis, DNA ; Spinal Cord/pathology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 13
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2002-06-22
    Beschreibung: In mammals, fertilization typically involves the ovulation of one or a few eggs at one end of the female reproductive tract and the entry of millions of sperm at the other. Given this disparity in numbers, it might be expected that the more precious commodity-eggs-would be subject to more stringent quality-control mechanisms. However, information from engineered mutations of meiotic genes suggests just the opposite. Specifically, the available mutants demonstrate striking sexual dimorphism in response to meiotic disruption; for example, faced with adversity, male meiosis grinds to a halt, whereas female meiosis soldiers on. This female "robustness" comes with a cost, however, because aneuploidy appears to be increased in the resultant oocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hunt, Patricia A -- Hassold, Terry J -- HD21341/HD/NICHD NIH HHS/ -- HD31866/HD/NICHD NIH HHS/ -- HD37502/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2002 Jun 21;296(5576):2181-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Case Western Reserve University, Cleveland, OH 44106-4955, USA. pah13@po.cwru.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12077403" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aneuploidy ; Animals ; Cell Cycle ; Female ; Humans ; Male ; *Meiosis ; Mice ; Mutation ; Oocytes/*physiology ; *Oogenesis ; Prophase ; Proteins/genetics/metabolism ; Sex Characteristics ; Spermatocytes/*physiology ; *Spermatogenesis
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 14
    Publikationsdatum: 2003-12-13
    Beschreibung: Even though human and chimpanzee gene sequences are nearly 99% identical, sequence comparisons can nevertheless be highly informative in identifying biologically important changes that have occurred since our ancestral lineages diverged. We analyzed alignments of 7645 chimpanzee gene sequences to their human and mouse orthologs. These three-species sequence alignments allowed us to identify genes undergoing natural selection along the human and chimp lineage by fitting models that include parameters specifying rates of synonymous and nonsynonymous nucleotide substitution. This evolutionary approach revealed an informative set of genes with significantly different patterns of substitution on the human lineage compared with the chimpanzee and mouse lineages. Partitions of genes into inferred biological classes identified accelerated evolution in several functional classes, including olfaction and nuclear transport. In addition to suggesting adaptive physiological differences between chimps and humans, human-accelerated genes are significantly more likely to underlie major known Mendelian disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, Andrew G -- Glanowski, Stephen -- Nielsen, Rasmus -- Thomas, Paul D -- Kejariwal, Anish -- Todd, Melissa A -- Tanenbaum, David M -- Civello, Daniel -- Lu, Fu -- Murphy, Brian -- Ferriera, Steve -- Wang, Gary -- Zheng, Xianqgun -- White, Thomas J -- Sninsky, John J -- Adams, Mark D -- Cargill, Michele -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1960-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671302" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Active Transport, Cell Nucleus/genetics ; Amino Acids/metabolism ; Animals ; Biological Evolution ; Computational Biology ; *Evolution, Molecular ; Female ; Genes ; Genetic Diseases, Inborn/genetics ; *Genome ; *Genome, Human ; Humans ; Likelihood Functions ; Male ; Mice/genetics ; Models, Genetic ; Models, Statistical ; Mutation ; Pan troglodytes/*genetics ; Phylogeny ; Proteins/chemistry/genetics ; Pseudogenes ; Receptors, Odorant/genetics ; *Selection, Genetic ; Sequence Alignment ; Sequence Homology, Nucleic Acid ; Signal Transduction/genetics ; Smell/genetics ; Species Specificity
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 15
    Publikationsdatum: 2005-11-19
    Beschreibung: The attack on the World Trade Center on 9/11/2001 challenged current approaches to forensic DNA typing methods. The large number of victims and the extreme thermal and physical conditions of the site necessitated special approaches to the DNA-based identification. Because of these and many additional challenges, new procedures were created or modified from routine forensic protocols. This effort facilitated the identification of 1594 of the 2749 victims. In this Policy Forum, the authors, who were were members of the World Trade Center Kinship and Data Analysis Panel, review the lessons of the attack response from the perspective of DNA forensic identification and suggest policies and procedures for future mass disasters or large-scale terrorist attacks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biesecker, Leslie G -- Bailey-Wilson, Joan E -- Ballantyne, Jack -- Baum, Howard -- Bieber, Frederick R -- Brenner, Charles -- Budowle, Bruce -- Butler, John M -- Carmody, George -- Conneally, P Michael -- Duceman, Barry -- Eisenberg, Arthur -- Forman, Lisa -- Kidd, Kenneth K -- Leclair, Benoit -- Niezgoda, Steven -- Parsons, Thomas J -- Pugh, Elizabeth -- Shaler, Robert -- Sherry, Stephen T -- Sozer, Amanda -- Walsh, Anne -- New York, N.Y. -- Science. 2005 Nov 18;310(5751):1122-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293742" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Dna ; *DNA Fingerprinting/methods ; DNA, Mitochondrial ; Disaster Planning ; Family ; Female ; Forecasting ; Genetic Markers ; Humans ; Male ; *September 11 Terrorist Attacks ; Specimen Handling ; United States
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 16
    Publikationsdatum: 2004-07-27
    Beschreibung: Psychologists, economists, and advertising moguls have long known that human decision-making is strongly influenced by the behavior of others. A rapidly accumulating body of evidence suggests that the same is true in animals. Individuals can use information arising from cues inadvertently produced by the behavior of other individuals with similar requirements. Many of these cues provide public information about the quality of alternatives. The use of public information is taxonomically widespread and can enhance fitness. Public information can lead to cultural evolution, which we suggest may then affect biological evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Danchin, Etienne -- Giraldeau, Luc-Alain -- Valone, Thomas J -- Wagner, Richard H -- New York, N.Y. -- Science. 2004 Jul 23;305(5683):487-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.P.M.C. CNRS-UMR7625, Bat A-7e etage-Case 237, 7 quai Saint Bernard, 75252 Paris Cedex 05, France. edanchin@snv.jussieu.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15273386" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Behavior, Animal ; Biological Evolution ; Cues ; *Cultural Evolution ; *Decision Making ; Environment ; Feeding Behavior ; Female ; Genes ; Humans ; Male ; Reproduction ; Sexual Behavior, Animal
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 17
    Publikationsdatum: 2004-05-01
    Beschreibung: Receptor tyrosine kinase genes were sequenced in non-small cell lung cancer (NSCLC) and matched normal tissue. Somatic mutations of the epidermal growth factor receptor gene EGFR were found in 15of 58 unselected tumors from Japan and 1 of 61 from the United States. Treatment with the EGFR kinase inhibitor gefitinib (Iressa) causes tumor regression in some patients with NSCLC, more frequently in Japan. EGFR mutations were found in additional lung cancer samples from U.S. patients who responded to gefitinib therapy and in a lung adenocarcinoma cell line that was hypersensitive to growth inhibition by gefitinib, but not in gefitinib-insensitive tumors or cell lines. These results suggest that EGFR mutations may predict sensitivity to gefitinib.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paez, J Guillermo -- Janne, Pasi A -- Lee, Jeffrey C -- Tracy, Sean -- Greulich, Heidi -- Gabriel, Stacey -- Herman, Paula -- Kaye, Frederic J -- Lindeman, Neal -- Boggon, Titus J -- Naoki, Katsuhiko -- Sasaki, Hidefumi -- Fujii, Yoshitaka -- Eck, Michael J -- Sellers, William R -- Johnson, Bruce E -- Meyerson, Matthew -- New York, N.Y. -- Science. 2004 Jun 4;304(5676):1497-500. Epub 2004 Apr 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Medical Oncology and Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15118125" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenocarcinoma/drug therapy/genetics/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Amino Acid Substitution ; Antineoplastic Agents/pharmacology/therapeutic use ; Carcinoma, Non-Small-Cell Lung/drug therapy/*genetics/metabolism ; Cell Line, Tumor ; Controlled Clinical Trials as Topic ; Enzyme Inhibitors/pharmacology/therapeutic use ; Female ; *Genes, erbB-1 ; Humans ; Japan ; Lung Neoplasms/drug therapy/*genetics/metabolism ; Male ; Molecular Sequence Data ; *Mutation ; Mutation, Missense ; Phosphorylation ; Protein Conformation ; Protein Structure, Tertiary ; Quinazolines/pharmacology/*therapeutic use ; Receptor, Epidermal Growth Factor/*antagonists & ; inhibitors/chemistry/genetics/metabolism ; Sequence Deletion ; Treatment Outcome ; United States
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 18
    Publikationsdatum: 2005-05-14
    Beschreibung: Canary song is hierarchically structured: Short stereotyped syllables are repeated to form phrases, which in turn are arranged to form songs. This structure occurs even in the songs of young isolates, which suggests that innate rules govern canary song development. However, juveniles that had never heard normal song imitated abnormal synthetic songs with great accuracy, even when the tutor songs lacked phrasing. As the birds matured, imitated songs were reprogrammed to form typical canary phrasing. Thus, imitation and innate song constraints are separate processes that can be segregated in time: freedom in youth, rules in adulthood.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gardner, Timothy J -- Naef, Felix -- Nottebohm, Fernando -- MH18343/MH/NIMH NIH HHS/ -- MH63132/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2005 May 13;308(5724):1046-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Animal Behavior, Rockefeller University, New York, NY 10021, USA. tgardner@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15890887" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aging ; Animals ; Canaries/growth & development/*physiology ; Female ; *Imitative Behavior ; *Learning ; Male ; Memory ; Sexual Maturation ; Testosterone/pharmacology ; *Vocalization, Animal
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 19
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2005-05-21
    Beschreibung: Two distinct forms of consolidated associative memory are known in Drosophila: long-term memory and so-called anesthesia-resistant memory. Long-term memory is more stable, but unlike anesthesia-resistant memory, its formation requires protein synthesis. We show that flies induced to form long-term memory become more susceptible to extreme stress (such as desiccation). In contrast, induction of anesthesia-resistant memory had no detectable effect on desiccation resistance. This finding may help to explain why evolution has maintained anesthesia-resistant memory as another form of consolidated memory, distinct from long-term memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mery, Frederic -- Kawecki, Tadeusz J -- New York, N.Y. -- Science. 2005 May 20;308(5725):1148.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Ecology and Evolution, Department of Biology, University of Fribourg, Chemin du Musee 10, CH-1700 Fribourg, Switzerland. frederic.mery@unifr.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15905396" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biological Evolution ; Conditioning (Psychology) ; Drosophila Proteins/biosynthesis ; Drosophila melanogaster/*physiology ; Female ; Male ; Memory/*physiology ; Odors ; Starvation ; Water Deprivation
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 20
    Publikationsdatum: 2004-04-10
    Beschreibung: Susceptibility to asthma depends on variation at an unknown number of genetic loci. To identify susceptibility genes on chromosome 7p, we adopted a hierarchical genotyping design, leading to the identification of a 133-kilobase risk-conferring segment containing two genes. One of these coded for an orphan G protein-coupled receptor named GPRA (G protein-coupled receptor for asthma susceptibility), which showed distinct distribution of protein isoforms between bronchial biopsies from healthy and asthmatic individuals. In three cohorts from Finland and Canada, single nucleotide polymorphism-tagged haplotypes associated with high serum immunoglobulin E or asthma. The murine ortholog of GPRA was up-regulated in a mouse model of ovalbumin-induced inflammation. Together, these data implicate GPRA in the pathogenesis of atopy and asthma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laitinen, Tarja -- Polvi, Anne -- Rydman, Pia -- Vendelin, Johanna -- Pulkkinen, Ville -- Salmikangas, Paula -- Makela, Siru -- Rehn, Marko -- Pirskanen, Asta -- Rautanen, Anna -- Zucchelli, Marco -- Gullsten, Harriet -- Leino, Marina -- Alenius, Harri -- Petays, Tuula -- Haahtela, Tari -- Laitinen, Annika -- Laprise, Catherine -- Hudson, Thomas J -- Laitinen, Lauri A -- Kere, Juha -- New York, N.Y. -- Science. 2004 Apr 9;304(5668):300-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉GeneOS Limited, 00251 Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15073379" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Algorithms ; Alternative Splicing ; Animals ; Asthma/*genetics/metabolism ; Bronchi/chemistry/cytology ; Chromosomes, Human, Pair 7/*genetics ; Epithelial Cells/chemistry ; Female ; Finland ; Gene Expression ; Genes ; Genetic Linkage ; *Genetic Predisposition to Disease ; Genetic Variation ; Genotype ; *Haplotypes ; Humans ; Hypersensitivity/genetics/metabolism ; Immunoglobulin E/blood ; Inflammation/genetics ; Lung/metabolism ; Male ; Mice ; Myocytes, Smooth Muscle/chemistry ; Polymorphism, Single Nucleotide ; Quebec ; Receptors, G-Protein-Coupled/analysis/*genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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