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  • 1
    Publication Date: 2013-10-19
    Description: The chytrid fungus, Batrachochytrium dendrobatidis, causes chytridiomycosis and is a major contributor to global amphibian declines. Although amphibians have robust immune defenses, clearance of this pathogen is impaired. Because inhibition of host immunity is a common survival strategy of pathogenic fungi, we hypothesized that B. dendrobatidis evades clearance by inhibiting immune functions. We found that B. dendrobatidis cells and supernatants impaired lymphocyte proliferation and induced apoptosis; however, fungal recognition and phagocytosis by macrophages and neutrophils was not impaired. Fungal inhibitory factors were resistant to heat, acid, and protease. Their production was absent in zoospores and reduced by nikkomycin Z, suggesting that they may be components of the cell wall. Evasion of host immunity may explain why this pathogen has devastated amphibian populations worldwide.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3956111/" 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/PMC3956111/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fites, J Scott -- Ramsey, Jeremy P -- Holden, Whitney M -- Collier, Sarah P -- Sutherland, Danica M -- Reinert, Laura K -- Gayek, A Sophia -- Dermody, Terence S -- Aune, Thomas M -- Oswald-Richter, Kyra -- Rollins-Smith, Louise A -- 1K01HL103179-01/HL/NHLBI NIH HHS/ -- AI007281/AI/NIAID NIH HHS/ -- AI038296/AI/NIAID NIH HHS/ -- AI044924/AI/NIAID NIH HHS/ -- K01 HL103179/HL/NHLBI NIH HHS/ -- R01 AI038296/AI/NIAID NIH HHS/ -- R37 AI038296/AI/NIAID NIH HHS/ -- R56 AI044924/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 18;342(6156):366-9. doi: 10.1126/science.1243316.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Vanderbilt University, Nashville, TN 37235, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24136969" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoglycosides/pharmacology ; Amphibians/*immunology/*microbiology ; Animals ; Apoptosis/immunology ; Cell Proliferation ; Chytridiomycota/*pathogenicity ; Host-Pathogen Interactions/*immunology ; Lymphocytes/drug effects/*immunology/*microbiology ; Mycoses/immunology/*veterinary ; Spores, Fungal/pathogenicity ; Xenopus laevis
    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
    Publication Date: 2014-07-11
    Description: Emerging fungal pathogens pose a greater threat to biodiversity than any other parasitic group, causing declines of many taxa, including bats, corals, bees, snakes and amphibians. Currently, there is little evidence that wild animals can acquire resistance to these pathogens. Batrachochytrium dendrobatidis is a pathogenic fungus implicated in the recent global decline of amphibians. Here we demonstrate that three species of amphibians can acquire behavioural or immunological resistance to B. dendrobatidis. Frogs learned to avoid the fungus after just one B. dendrobatidis exposure and temperature-induced clearance. In subsequent experiments in which B. dendrobatidis avoidance was prevented, the number of previous exposures was a negative predictor of B. dendrobatidis burden on frogs and B. dendrobatidis-induced mortality, and was a positive predictor of lymphocyte abundance and proliferation. These results suggest that amphibians can acquire immunity to B. dendrobatidis that overcomes pathogen-induced immunosuppression and increases their survival. Importantly, exposure to dead fungus induced a similar magnitude of acquired resistance as exposure to live fungus. Exposure of frogs to B. dendrobatidis antigens might offer a practical way to protect pathogen-naive amphibians and facilitate the reintroduction of amphibians to locations in the wild where B. dendrobatidis persists. Moreover, given the conserved nature of vertebrate immune responses to fungi and the fact that many animals are capable of learning to avoid natural enemies, these results offer hope that other wild animal taxa threatened by invasive fungi might be rescued by management approaches based on herd immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4464781/" 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/PMC4464781/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McMahon, Taegan A -- Sears, Brittany F -- Venesky, Matthew D -- Bessler, Scott M -- Brown, Jenise M -- Deutsch, Kaitlin -- Halstead, Neal T -- Lentz, Garrett -- Tenouri, Nadia -- Young, Suzanne -- Civitello, David J -- Ortega, Nicole -- Fites, J Scott -- Reinert, Laura K -- Rollins-Smith, Louise A -- Raffel, Thomas R -- Rohr, Jason R -- R01 GM109499/GM/NIGMS NIH HHS/ -- R01GM109499/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Jul 10;511(7508):224-7. doi: 10.1038/nature13491.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] University of South Florida, Department of Integrative Biology, Tampa, Florida 33620, USA [2] University of Tampa, Department of Biology, Tampa, Florida 33606, USA [3]. ; University of South Florida, Department of Integrative Biology, Tampa, Florida 33620, USA. ; Allegheny College, Department of Biology, Meadville, Pennsylvania 16335, USA. ; Vanderbilt University, Biological Sciences Department, Nashville, Tennessee 37232, USA. ; Vanderbilt University, School of Medicine, Departments of Pathology, Microbiology and Immunology and Pediatrics, Nashville, Tennessee 37232, USA. ; 1] Vanderbilt University, Biological Sciences Department, Nashville, Tennessee 37232, USA [2] Vanderbilt University, School of Medicine, Departments of Pathology, Microbiology and Immunology and Pediatrics, Nashville, Tennessee 37232, USA. ; Oakland University, Department of Biology, Rochester, Michigan 48309, USA. ; 1] University of South Florida, Department of Integrative Biology, Tampa, Florida 33620, USA [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25008531" target="_blank"〉PubMed〈/a〉
    Keywords: Amphibians/*immunology/*microbiology ; Animals ; Antigens, Fungal/immunology ; Cell Proliferation ; Chytridiomycota/*immunology ; Lymphocyte Count ; Lymphocytes/cytology ; Mycoses/*immunology/prevention & control ; Population Density ; Survival Analysis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2010-08-21
    Description: Individuals in socially monogamous species may participate in copulations outside of the pair bond, resulting in extra-pair offspring. Although males benefit from such extra-pair behavior if they produce more offspring, the adaptive function of infidelity to females remains elusive. Here we show that female participation in extra-pair copulations, combined with a genetically loaded process of sperm competition, enables female finches to target genes that are optimally compatible with their own to ensure fertility and optimize offspring viability. Such female behavior, along with the postcopulatory processes demonstrated here, may provide an adaptive function of female infidelity in socially monogamous animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pryke, Sarah R -- Rollins, Lee A -- Griffith, Simon C -- New York, N.Y. -- Science. 2010 Aug 20;329(5994):964-7. doi: 10.1126/science.1192407.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Macquarie University, Sydney, NSW 2109, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20724639" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Biological ; Animals ; Female ; Fertilization/genetics ; Finches/genetics/*physiology ; Genes ; Male ; *Mating Preference, Animal ; *Pair Bond ; Selection, Genetic ; Spermatozoa/*physiology
    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: 2015-07-09
    Description: Alloparental care by distant/nonkin that accrue few kin-selected benefits requires direct fitness benefits to evolve. The pay-to-stay hypothesis, under which helpers contribute to alloparental care to avoid being expelled from the group by dominant individuals, offers one such explanation. Here, we investigated 2 key predictions derived from the pay-to-stay hypothesis using the chestnut-crowed babbler, Pomatostomus ruficeps , a cooperatively breeding bird where helping by distant/nonkin is common (18% of nonbreeding helpers). First, we found no indication that distant or nonkin male helpers advertised their contributions toward the primary male breeder. Helpers unrelated to both breeders were unresponsive to provisioning rates of the dominant male, whereas helpers that were related to either the breeding male or to both members of the pair were responsive. In addition, unrelated male helpers did not advertise their contributions to provisioning by disproportionately synchronizing their provisioning events with those of the primary male breeder or by provisioning nestlings immediately after him. Second, no helper, irrespective of its relatedness to the dominant breeders, received aggression when released back into the group following temporary removal for 1–2 days. We therefore find no compelling support for the hypothesis that pay-to-stay mechanisms account for the cooperative behavior of unrelated males in chestnut-crowned babblers.
    Print ISSN: 1045-2249
    Electronic ISSN: 1465-7279
    Topics: Biology
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  • 5
    Publication Date: 2016-03-04
    Description: Mitochondria are critical for life, yet their underlying evolutionary biology is poorly understood. In particular, little is known about interaction between two levels of evolution: between individuals and within individuals (competition between cells, mitochondria or mitochondrial DNA molecules). Rapid evolution is suspected to occur frequently in mitochondrial DNA, whose maternal inheritance predisposes advantageous mutations to sweep rapidly though populations. Rapid evolution is also predicted in response to changed selection regimes after species invasion or removal of pathogens or competitors. Here, using empirical and simulated data from a model invasive bird species, we provide the first demonstration of rapid selection on the mitochondrial genome within individuals in the wild. Further, we show differences in mitochondrial DNA copy number associated with competing genetic variants, which may provide a mechanism for selection. We provide evidence for three rarely documented phenomena: selection associated with mitochondrial DNA abundance, selection on the mitochondrial control region, and contemporary selection during invasion.
    Print ISSN: 0737-4038
    Electronic ISSN: 1537-1719
    Topics: Biology
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  • 6
    Publication Date: 2016-09-07
    Print ISSN: 0025-3162
    Electronic ISSN: 1432-1793
    Topics: Biology
    Published by Springer
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  • 7
    Publication Date: 2015-06-01
    Print ISSN: 0269-8463
    Electronic ISSN: 1365-2435
    Topics: Biology
    Published by Wiley on behalf of British Ecological Society.
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