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  • 1
    Publication Date: 2000-02-26
    Description: Most types of antibiotic resistance impose a biological cost on bacterial fitness. These costs can be compensated, usually without loss of resistance, by second-site mutations during the evolution of the resistant bacteria in an experimental host or in a laboratory medium. Different fitness-compensating mutations were selected depending on whether the bacteria evolved through serial passage in mice or in a laboratory medium. This difference in mutation spectra was caused by either a growth condition-specific formation or selection of the compensated mutants. These results suggest that bacterial evolution to reduce the costs of antibiotic resistance can take different trajectories within and outside a host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bjorkman, J -- Nagaev, I -- Berg, O G -- Hughes, D -- Andersson, D I -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1479-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacteriology, Swedish Institute for Infectious Disease Control, S-171 82 Solna, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10688795" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Anti-Bacterial Agents/*pharmacology ; *Antiporters ; Carrier Proteins/genetics ; Culture Media ; Drug Resistance, Microbial/*genetics ; Escherichia coli Proteins ; Evolution, Molecular ; Female ; Fusidic Acid/pharmacology ; Membrane Proteins/genetics ; Mice ; Mice, Inbred BALB C ; *Mutation ; Peptide Elongation Factor G/genetics ; Ribosomal Proteins/genetics ; Salmonella typhimurium/*drug effects/*genetics/growth & development/metabolism ; Selection, Genetic ; Serial Passage ; Streptomycin/pharmacology ; Suppression, Genetic
    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: 2001-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alverson, K -- Bradley, R -- Briffa, K -- Cole, J -- Hughes, M -- Larocque, I -- Pedersen, T -- Thompson, L -- Tudhope, S -- New York, N.Y. -- Science. 2001 Jul 6;293(5527):47-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11444288" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon Dioxide/metabolism ; *Climate ; Cnidaria/physiology ; Conservation of Natural Resources ; Greenhouse Effect ; Humans ; Ice ; Oceans and Seas ; Rain ; Seawater/analysis/chemistry ; Specimen Handling/*methods ; Temperature ; Time Factors ; Trees/growth & development/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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  • 3
    Publication Date: 2001-07-28
    Description: Ecological extinction caused by overfishing precedes all other pervasive human disturbance to coastal ecosystems, including pollution, degradation of water quality, and anthropogenic climate change. Historical abundances of large consumer species were fantastically large in comparison with recent observations. Paleoecological, archaeological, and historical data show that time lags of decades to centuries occurred between the onset of overfishing and consequent changes in ecological communities, because unfished species of similar trophic level assumed the ecological roles of overfished species until they too were overfished or died of epidemic diseases related to overcrowding. Retrospective data not only help to clarify underlying causes and rates of ecological change, but they also demonstrate achievable goals for restoration and management of coastal ecosystems that could not even be contemplated based on the limited perspective of recent observations alone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jackson, J B -- Kirby, M X -- Berger, W H -- Bjorndal, K A -- Botsford, L W -- Bourque, B J -- Bradbury, R H -- Cooke, R -- Erlandson, J -- Estes, J A -- Hughes, T P -- Kidwell, S -- Lange, C B -- Lenihan, H S -- Pandolfi, J M -- Peterson, C H -- Steneck, R S -- Tegner, M J -- Warner, R R -- New York, N.Y. -- Science. 2001 Jul 27;293(5530):629-37.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Scripps Institution of Oceanography, University of California, San Diego, La Jolla, CA 92093-0244, USA. jbcj@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11474098" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Archaeology ; Bacteria ; Cnidaria ; Conservation of Natural Resources ; *Ecosystem ; Eutrophication ; *Fishes ; Geologic Sediments ; Humans ; *Marine Biology ; Seaweed ; Shellfish ; Time Factors
    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: 2002-05-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baird, Andrew H -- Bellwood, David R -- Connell, Joseph H -- Cornell, Howard V -- Hughes, Terry P -- Karlson, Ronald H -- Rosen, Brian R -- New York, N.Y. -- Science. 2002 May 10;296(5570):1026-8; author reply 1026-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12004903" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Climate ; *Cnidaria ; *Conservation of Natural Resources ; *Ecosystem ; Nephropidae ; Seawater ; Snails
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-05-26
    Description: Tropical reef fishes and corals exhibit highly predictable patterns of taxonomic composition across the Indian and Pacific Oceans. Despite steep longitudinal and latitudinal gradients in total species richness, the composition of these key taxa is constrained within a remarkably narrow range of values. Regional-scale variation in reef biodiversity is best explained by large-scale patterns in the availability of shallow-water habitat. Once habitat area is accounted for, there is surprisingly little residual effect of latitude or longitude. Low-diversity regions are most vulnerable to human impacts such as global warming, underscoring the urgent need for integrated management at multinational scales.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bellwood, D R -- Hughes, T P -- New York, N.Y. -- Science. 2001 May 25;292(5521):1532-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Coral Reef Biodiversity, Department of Marine Biology, James Cook University, Townsville, Qld 4811, Australia. david.bellwood@jcu.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11375488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cnidaria/classification/physiology ; Conservation of Natural Resources ; *Ecosystem ; *Fishes/classification/physiology ; Geography ; Greenhouse Effect ; Indian Ocean ; Pacific Ocean ; Temperature
    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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  • 6
    Publication Date: 2003-08-16
    Description: Degradation of coral reef ecosystems began centuries ago, but there is no global summary of the magnitude of change. We compiled records, extending back thousands of years, of the status and trends of seven major guilds of carnivores, herbivores, and architectural species from 14 regions. Large animals declined before small animals and architectural species, and Atlantic reefs declined before reefs in the Red Sea and Australia, but the trajectories of decline were markedly similar worldwide. All reefs were substantially degraded long before outbreaks of coral disease and bleaching. Regardless of these new threats, reefs will not survive without immediate protection from human exploitation over large spatial scales.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pandolfi, John M -- Bradbury, Roger H -- Sala, Enric -- Hughes, Terence P -- Bjorndal, Karen A -- Cooke, Richard G -- McArdle, Deborah -- McClenachan, Loren -- Newman, Marah J H -- Paredes, Gustavo -- Warner, Robert R -- Jackson, Jeremy B C -- New York, N.Y. -- Science. 2003 Aug 15;301(5635):955-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Paleobiology, MRC-121, National Museum of Natural History, Post Office Box 37012, Smithsonian Institution, Washington, DC 20013-7012, USA. pandolfi.john@nmnh.si.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920296" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/*growth & development ; Conservation of Natural Resources ; Culture ; *Ecosystem ; Humans ; Population Dynamics ; Principal Component Analysis ; Time Factors
    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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  • 7
    Publication Date: 2003-08-16
    Description: The diversity, frequency, and scale of human impacts on coral reefs are increasing to the extent that reefs are threatened globally. Projected increases in carbon dioxide and temperature over the next 50 years exceed the conditions under which coral reefs have flourished over the past half-million years. However, reefs will change rather than disappear entirely, with some species already showing far greater tolerance to climate change and coral bleaching than others. International integration of management strategies that support reef resilience need to be vigorously implemented, and complemented by strong policy decisions to reduce the rate of global warming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, T P -- Baird, A H -- Bellwood, D R -- Card, M -- Connolly, S R -- Folke, C -- Grosberg, R -- Hoegh-Guldberg, O -- Jackson, J B C -- Kleypas, J -- Lough, J M -- Marshall, P -- Nystrom, M -- Palumbi, S R -- Pandolfi, J M -- Rosen, B -- Roughgarden, J -- New York, N.Y. -- Science. 2003 Aug 15;301(5635):929-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Coral Reef Biodiversity, James Cook University, Townsville, Qld 4811, Australia. terry.hughes@jcu.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920289" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Biological ; Animals ; Anthozoa/growth & development/*physiology ; *Climate ; *Conservation of Natural Resources ; *Ecosystem ; Environment ; Fishes ; Greenhouse Effect ; Humans
    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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  • 8
    Publication Date: 2011-08-24
    Description: Arachidonic acid (AA) is the precursor for prostaglandin E2 (PGE2) synthesis and increases growth of prostate cancer cells. To further elucidate the mechanisms involved in AA-induced prostate cell growth, induction of c-fos expression by AA was investigated in a human prostate cancer cell line, PC-3. c-fos mRNA was induced shortly after addition of AA, along with a remarkable increase in PGE2 production. c-fos expression and PGE2 production induced by AA was blocked by a cyclo-oxygenase inhibitor, flurbiprofen, suggesting that PGE2 mediated c-fos induction. Protein kinase A (PKA) inhibitor H-89 abolished induction of c-fos expression by AA, and partially inhibited PGE2 production. Protein kinase C (PKC) inhibitor GF109203X had no significant effect on c-fos expression or PGE2 production. Expression of prostaglandin (EP) receptors, which mediate signal transduction from PGE2 to the cells, was examined by reverse transcription polymerase chain reaction in several human prostate cell lines. EP4 and EP2, which are coupled to the PKA signalling pathway, were expressed in all cells tested. Expression of EP1, which activates the PKC pathway, was not detected. The current study showed that induction of the immediate early gene c-fos by AA is mediated by PGE2, which activates the PKA pathway via the EP2/4 receptor in the PC-3 cells.
    Keywords: Life Sciences (General)
    Type: British journal of cancer (ISSN 0007-0920); Volume 82; 12; 2000-6
    Format: text
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  • 9
    Publication Date: 2011-08-24
    Description: The mechanism by which the proto-oncogene, c-fos, is up-regulated in response to PGE2 in the mouse osteoblastic (MC3T3-E1) cell line was investigated using RT-PCR. c-fos messenger RNA up-regulation by dmPGE2 is rapid, starting 10 min post stimulation, and transient. The specific protein kinase A (PKA) inhibitor, H89, inhibited c-fos induction. Moreover, down-regulation of protein kinase C (PKC) activity by chronic TPA treatment had no effect on the induction of c-fos by dmPGE2. We conclude that up-regulation of c-fos by dmPGE2 is primarily dependent on PKA in MC3T3-E1 osteoblasts. In S49 lymphoma wild-type but not S49 cyc- cells, which are deficient in cAMP signaling, dmPGE2 up-regulates c-fos and increases cell growth compared with unstimulated cells. Thus in S49 lymphoma cells, c-fos induction by PGE2 is also dependent on cAMP signaling. The minimal c-fos promoter region required for dmPGE2-induced expression was identified by transfecting c-fos promoter deletion constructs coupled to the chloramphenicol acetyltransferase (CAT) reporter gene into Vero cells. Transfection of a plasmid containing 99 bp c-fos proximal promoter was sufficient to direct c-fos/CAT expression following stimulation with dmPGE2. Because induction of c-fos is mediated by cAMP, these data are consistent with activation of c-fos via the CRE/ATF cis element.
    Keywords: Life Sciences (General)
    Type: Endocrinology (ISSN 0013-7227); Volume 141; 1; 291-8
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  • 10
    Publication Date: 2011-08-24
    Description: It has been proposed that the omega-6 fatty acids increase the rate of tumor growth. Here we test that hypothesis in the PC-3 human prostate tumor. We found that the essential fatty acids, linoleic acid (LA) and arachidonic acid (AA), and the AA metabolite PGE(2) stimulate tumor growth while oleic acid (OA) and the omega-3 fatty acid, eicosapentaenoic acid (EPA) inhibited growth. In examining the role of AA in growth response, we extended our studies to analyze changes in early gene expression induced by AA. We demonstrate that c-fos expression is increased within minutes of addition in a dose-dependent manner. Moreover, the immediate early gene cox-2 is also increased in the presence of AA in a dose-dependent manner, while the constitutive cox-1 message was not increased. Three hours after exposure to AA, the synthesis of PGE(2) via COX-2 was also increased. Previous studies have demonstrated that AA was primarily delivered by low density lipoprotein (LDL) via its receptor (LDLr). Since it is known that hepatomas, acute myelogenous leukemia and colorectal tumors lack normal cholesterol feedback, we examined the role of the LDLr in growth regulation of the PC-3 prostate cancer cells. Analysis of ldlr mRNA expression and LDLr function demonstrated that human PC-3 prostate cancer cells lack normal feedback regulation. While exogenous LDL caused a significant stimulation of cell growth and PGE(2) synthesis, no change was seen in regulation of the LDLr by LDL. Taken together, these data show that normal cholesterol feedback of ldlr message and protein is lost in prostate cancer. These data suggest that unregulated over-expression of LDLr in tumor cells would permit increased availability of AA, which induces immediate early genes c-fos and cox-2 within minutes of uptake.
    Keywords: Life Sciences (General)
    Type: Carcinogenesis (ISSN 0143-3334); Volume 22; 5; 701-7
    Format: text
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