ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Trophic structure and community stability in an overfished ecosystem (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-22
    Description: Since the collapse of the pelagic fisheries off southwest Africa in the late 1960s, jellyfish biomass has increased and the structure of the Benguelan fish community has shifted, making the bearded goby (Sufflogobius bibarbatus) the new predominant prey species. Despite increased predation pressure and a harsh environment, the gobies are thriving. Here we show that physiological adaptations and antipredator and foraging behaviors underpin the success of these fish. In particular, body-tissue isotope signatures reveal that gobies consume jellyfish and sulphidic diatomaceous mud, transferring "dead-end" resources back into the food chain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Utne-Palm, Anne C -- Salvanes, Anne G V -- Currie, Bronwen -- Kaartvedt, Stein -- Nilsson, Goran E -- Braithwaite, Victoria A -- Stecyk, Jonathan A W -- Hundt, Matthias -- van der Bank, Megan -- Flynn, Bradley -- Sandvik, Guro K -- Klevjer, Thor A -- Sweetman, Andrew K -- Bruchert, Volker -- Pittman, Karin -- Peard, Kathleen R -- Lunde, Ida G -- Strandabo, Ronnaug A U -- Gibbons, Mark J -- New York, N.Y. -- Science. 2010 Jul 16;329(5989):333-6. doi: 10.1126/science.1190708.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Bergen, Bergen, Norway. anne.palm@bio.uib.no〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647468" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Anaerobiosis ; Animals ; Bacteria ; Behavior, Animal ; Biomass ; Cardiovascular Physiological Phenomena ; Digestion ; *Ecosystem ; Feeding Behavior ; Fisheries ; Fishes/physiology ; *Food Chain ; Geologic Sediments/microbiology ; Hydrogen Sulfide/analysis ; Namibia ; Oxygen/analysis ; Oxygen Consumption ; Perciformes/*physiology ; Population Dynamics ; Predatory Behavior ; *Scyphozoa ; Seawater/chemistry
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Intravascular danger signals guide neutrophils to sites of sterile inflammation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: Neutrophils are recruited from the blood to sites of sterile inflammation, where they contribute to wound healing but may also cause tissue damage. By using spinning disk confocal intravital microscopy, we examined the kinetics and molecular mechanisms of neutrophil recruitment to sites of focal hepatic necrosis in vivo. Adenosine triphosphate released from necrotic cells activated the Nlrp3 inflammasome to generate an inflammatory microenvironment that alerted circulating neutrophils to adhere within liver sinusoids. Subsequently, generation of an intravascular chemokine gradient directed neutrophil migration through healthy tissue toward foci of damage. Lastly, formyl-peptide signals released from necrotic cells guided neutrophils through nonperfused sinusoids into the injury. Thus, dynamic in vivo imaging revealed a multistep hierarchy of directional cues that guide neutrophil localization to sites of sterile inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, Braedon -- Pittman, Keir -- Menezes, Gustavo B -- Hirota, Simon A -- Slaba, Ingrid -- Waterhouse, Christopher C M -- Beck, Paul L -- Muruve, Daniel A -- Kubes, Paul -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):362-6. doi: 10.1126/science.1195491.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Research Group, University of Calgary, Alberta T2N 4N1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947763" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Carrier Proteins/metabolism ; Cell Adhesion ; Chemokine CXCL2/metabolism ; Chemokines/metabolism ; Chemotaxis, Leukocyte ; Cues ; Endothelium, Vascular/physiology ; Inflammation/*immunology/metabolism/*pathology ; Kinetics ; Liver/blood supply/*immunology/metabolism/*pathology ; Liver Diseases/*immunology/metabolism/*pathology ; Macrophage-1 Antigen/physiology ; Mice ; Microscopy/methods ; Microscopy, Confocal ; Microvessels/physiology ; Necrosis ; *Neutrophil Infiltration ; Neutrophils/physiology ; Peptides/metabolism ; Receptors, Formyl Peptide/metabolism ; Receptors, Interleukin-8B/metabolism ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2X7 ; Signal Transduction
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Nucleoside reverse transcriptase inhibitors possess intrinsic anti-inflammatory activity (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-11-22
    Description: Nucleoside reverse transcriptase inhibitors (NRTIs) are mainstay therapeutics for HIV that block retrovirus replication. Alu (an endogenous retroelement that also requires reverse transcriptase for its life cycle)-derived RNAs activate P2X7 and the NLRP3 inflammasome to cause cell death of the retinal pigment epithelium in geographic atrophy, a type of age-related macular degeneration. We found that NRTIs inhibit P2X7-mediated NLRP3 inflammasome activation independent of reverse transcriptase inhibition. Multiple approved and clinically relevant NRTIs prevented caspase-1 activation, the effector of the NLRP3 inflammasome, induced by Alu RNA. NRTIs were efficacious in mouse models of geographic atrophy, choroidal neovascularization, graft-versus-host disease, and sterile liver inflammation. Our findings suggest that NRTIs are ripe for drug repurposing in P2X7-driven diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4274127/" 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/PMC4274127/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fowler, Benjamin J -- Gelfand, Bradley D -- Kim, Younghee -- Kerur, Nagaraj -- Tarallo, Valeria -- Hirano, Yoshio -- Amarnath, Shoba -- Fowler, Daniel H -- Radwan, Marta -- Young, Mark T -- Pittman, Keir -- Kubes, Paul -- Agarwal, Hitesh K -- Parang, Keykavous -- Hinton, David R -- Bastos-Carvalho, Ana -- Li, Shengjian -- Yasuma, Tetsuhiro -- Mizutani, Takeshi -- Yasuma, Reo -- Wright, Charles -- Ambati, Jayakrishna -- BB/J017345/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- DP1 GM114862/GM/NIGMS NIH HHS/ -- DP1GM114862/DP/NCCDPHP CDC HHS/ -- K99 EY024336/EY/NEI NIH HHS/ -- K99EY024336/EY/NEI NIH HHS/ -- P30EY003040/EY/NEI NIH HHS/ -- R01 EY018350/EY/NEI NIH HHS/ -- R01 EY018836/EY/NEI NIH HHS/ -- R01 EY020672/EY/NEI NIH HHS/ -- R01 EY022238/EY/NEI NIH HHS/ -- R01 EY024068/EY/NEI NIH HHS/ -- R01EY001545/EY/NEI NIH HHS/ -- R01EY018350/EY/NEI NIH HHS/ -- R01EY018836/EY/NEI NIH HHS/ -- R01EY020672/EY/NEI NIH HHS/ -- R01EY022238/EY/NEI NIH HHS/ -- R01EY024068/EY/NEI NIH HHS/ -- T32HL091812/HL/NHLBI NIH HHS/ -- TL1 RR033172/RR/NCRR NIH HHS/ -- TL1 TR000115/TR/NCATS NIH HHS/ -- UL1 RR033173/RR/NCRR NIH HHS/ -- UL1 TR000117/TR/NCATS NIH HHS/ -- UL1RR033173/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2014 Nov 21;346(6212):1000-3. doi: 10.1126/science.1261754.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ophthalmology and Visual Sciences, University of Kentucky, Lexington, KY 40536, USA. Department of Physiology, University of Kentucky, Lexington, KY 40536, USA. ; Department of Ophthalmology and Visual Sciences, University of Kentucky, Lexington, KY 40536, USA. Department of Microbiology, Immunology, and Human Genetics, University of Kentucky, Lexington, KY 40536, USA. Department of Biomedical Engineering, University of Kentucky, Lexington, KY 40536, USA. ; Department of Ophthalmology and Visual Sciences, University of Kentucky, Lexington, KY 40536, USA. ; Department of Ophthalmology and Visual Sciences, University of Kentucky, Lexington, KY 40536, USA. Angiogenesis Lab, Institute of Genetics and Biophysics, CNR, Naples, Italy. ; Experimental Transplantation and Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; School of Biosciences, Cardiff University, Cardiff CF10 3AX, UK. ; Immunology Research Group, University of Calgary, Calgary, Alberta T2N 4N1, Canada. ; Chapman University School of Pharmacy, 9401 Jeronimo Road, Harry and Diane Rinker Health Science Campus, Irvine, CA 92618, USA. ; Departments of Pathology and Ophthalmology, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. ; Department of Ophthalmology and Visual Sciences, University of Kentucky, Lexington, KY 40536, USA. Department of Physiology, University of Kentucky, Lexington, KY 40536, USA. jamba2@email.uky.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25414314" target="_blank"〉PubMed〈/a〉
    Keywords: Alu Elements ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/*pharmacology/therapeutic use ; Apoptosis/drug effects ; Carrier Proteins/metabolism ; Caspase 1/metabolism ; Choroidal Neovascularization/drug therapy ; Disease Models, Animal ; Geographic Atrophy/drug therapy ; Graft vs Host Disease/drug therapy ; Hepatitis/drug therapy ; Inflammasomes/*drug effects ; Liver/drug effects ; Mice ; Receptors, Purinergic P2X7/metabolism ; Retinal Pigment Epithelium/drug effects/metabolism/physiology ; Reverse Transcriptase Inhibitors/*pharmacology/therapeutic use
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...