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  • 1
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    Trade-offs and triple-bottom-line solutions [Sustainability Science] (2013)
    National Academy of Sciences
    Details
    Publication Date: 2013-04-10
    Description: Triple–bottom-line outcomes from resource management and conservation, where conservation goals and equity in social outcomes are maximized while overall costs are minimized, remain a highly sought-after ideal. However, despite widespread recognition of the importance that equitable distribution of benefits or costs across society can play in conservation success, little formal...
    Keywords: Sustainability Science
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    Microbiology. Turning up the heat on Histoplasma capsulatum (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-02-24
    Description: Many fungal pathogens are opportunistic, that is, they infect individuals who have a compromised immune system. Histoplasma capsulatum is a common pathogenic fungus that lives happily inside the phagosomes of macrophages. As Klein explains in his Perspective, an important H. capsulatum virulence factor, CBP1, has been found, which mops up free calcium ions within the phagosome, enabling the yeast to live under calcium-poor conditions (Sebhgati et al.). Chelating calcium ions may also have the added benefit that when the phagosome fuses with the lysosome, destructive lysosomal enzymes that require calcium ions for activity remain inactive.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klein, B S -- New York, N.Y. -- Science. 2000 Nov 17;290(5495):1311-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Wisconsin-Madison, Madison, WI 53792, USA. bsklein@facstaff.wisc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11185407" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium-Binding Proteins/*genetics/*metabolism ; Cell Line ; Gene Targeting ; Genes, Fungal ; Histoplasma/genetics/growth & development/metabolism/*pathogenicity ; Histoplasmosis/microbiology ; Hydrogen-Ion Concentration ; Lung Diseases, Fungal/microbiology ; Macrophages/*microbiology ; Mice ; Mutagenesis ; Phagosomes/metabolism/microbiology ; Plasmids ; Recombination, Genetic ; Temperature ; Transformation, Genetic ; Virulence
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Recognition by human V gamma 9/V delta 2 T cells of a GroEL homolog on Daudi Burkitt's lymphoma cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-30
    Description: All human gamma delta T cells coexpressing the products of the variable (V) region T cell receptor (TCR) gene segments V gamma 9 and V delta 2 recognize antigens from mycobacterial extracts and Daudi cells. Exogenous and endogenous ligands on the cell surface, homologous to the groEL heat shock family, induced reactivities that resembled superantigen responses in this major subset of human peripheral blood gamma delta T cells. Stimulation of human V gamma 9/V delta 2 T cells is not restricted by human leukocyte antigens (HLA), including nonpolymorphic beta 2-microglobulin (beta 2M)-associated class Ib molecules. These data may be important for understanding the role of gamma delta T cells in autoimmunity and in responses to microorganisms and tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisch, P -- Malkovsky, M -- Kovats, S -- Sturm, E -- Braakman, E -- Klein, B S -- Voss, S D -- Morrissey, L W -- DeMars, R -- Welch, W J -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1269-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Oncology, University of Wisconsin, Madison 53792.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1978758" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen-Presenting Cells/immunology ; Antigens, Bacterial/*immunology ; Antigens, Neoplasm/*immunology ; Bacterial Proteins/*immunology ; Burkitt Lymphoma/*immunology ; Chaperonin 60 ; Clone Cells/immunology ; Escherichia coli/immunology ; Gene Expression ; Heat-Shock Proteins/*immunology ; Histocompatibility Antigens Class I/immunology ; Humans ; Immunoglobulin Variable Region/genetics/immunology ; Immunoglobulin delta-Chains/genetics/immunology ; Immunoglobulin gamma-Chains/genetics/immunology ; Immunosorbent Techniques ; Mycobacterium/immunology ; Receptors, Antigen, T-Cell/genetics/immunology ; T-Lymphocytes/*immunology ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Global control of dimorphism and virulence in fungi (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-29
    Description: Microbial pathogens that normally inhabit our environment can adapt to thrive inside mammalian hosts. There are six dimorphic fungi that cause disease worldwide, which switch from nonpathogenic molds in soil to pathogenic yeast after spores are inhaled and exposed to elevated temperature. Mechanisms that regulate this switch remain obscure. We show that a hybrid histidine kinase senses host signals and triggers the transition from mold to yeast. The kinase also regulates cell-wall integrity, sporulation, and expression of virulence genes in vivo. This global regulator shapes how dimorphic fungal pathogens adapt to the mammalian host, which has broad implications for treating and preventing systemic fungal disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nemecek, Julie C -- Wuthrich, Marcel -- Klein, Bruce S -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):583-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, University of Wisconsin Hospital and Clinics, Madison, WI 53792, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645097" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastomyces/cytology/enzymology/*genetics/*pathogenicity ; Blastomycosis/microbiology ; Coccidioides/enzymology/genetics/pathogenicity ; Fungal Proteins/genetics/physiology ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Genetic Complementation Test ; Histoplasma/enzymology/genetics/pathogenicity ; Histoplasmosis/microbiology ; Lung Diseases, Fungal/microbiology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutagenesis, Insertional ; Open Reading Frames ; Protein Kinases/chemistry/*genetics/*physiology ; RNA Interference ; Saccharomyces cerevisiae/genetics ; Soil Microbiology ; Spores, Fungal/physiology ; Temperature ; Virulence/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Pulmonary neuroendocrine cells amplify allergic asthma responses (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-06-08
    Description: Pulmonary neuroendocrine cells (PNECs) are rare airway epithelial cells whose function is poorly understood. Here we show that Ascl1 -mutant mice that have no PNECs exhibit severely blunted mucosal type 2 response in models of allergic asthma. PNECs reside in close proximity to group 2 innate lymphoid cells (ILC2s) near airway branch points. PNECs act through calcitonin gene-related peptide (CGRP) to stimulate ILC2s and elicit downstream immune responses. In addition, PNECs act through the neurotransmitter -aminobutyric acid (GABA) to induce goblet cell hyperplasia. The instillation of a mixture of CGRP and GABA in Ascl1 -mutant airways restores both immune and goblet cell responses. In accordance, lungs from human asthmatics show increased PNECs. These findings demonstrate that the PNEC-ILC2 neuroimmunological modules function at airway branch points to amplify allergic asthma responses.
    Keywords: Immunology, Medicine, Diseases, Online Only
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    The balance between immunity and inflammation (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2017-09-08
    Keywords: Immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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