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  • Articles  (22)
  • Medicine  (12)
  • Energy, Environment Protection, Nuclear Power Engineering  (10)
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  • Articles  (22)
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  • 1
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    Phenological sensitivity to climate across taxa and trophic levels (2016)
    Springer Nature
    In: Nature
    Details
    Publication Date: 2016-07-14
    Description: Phenological sensitivity to climate across taxa and trophic levels Nature 535, 7611 (2016). doi:10.1038/nature18608 Authors: Stephen J. Thackeray, Peter A. Henrys, Deborah Hemming, James R. Bell, Marc S. Botham, Sarah Burthe, Pierre Helaouet, David G. Johns, Ian D. Jones, David I. Leech, Eleanor B. Mackay, Dario Massimino, Sian Atkinson, Philip J. Bacon, Tom M. Brereton, Laurence Carvalho, Tim H. Clutton-Brock, Callan Duck, Martin Edwards, J. Malcolm Elliott, Stephen J. G. Hall, Richard Harrington, James W. Pearce-Higgins, Toke T. Høye, Loeske E. B. Kruuk, Josephine M. Pemberton, Tim H. Sparks, Paul M. Thompson, Ian White, Ian J. Winfield & Sarah Wanless Differences in phenological responses to climate change among species can desynchronise ecological interactions and thereby threaten ecosystem function. To assess these threats, we must quantify the relative impact of climate change on species at different trophic levels. Here, we apply a Climate Sensitivity Profile approach
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 2
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    Maintaining northern peatland ecosystems in a changing climate: effects of soil moisture, drainage and drain blocking on craneflies (2011)
    Wiley
    Details
    Publication Date: 2011-03-02
    Description: The capacity of peatlands in the northern hemisphere to provide carbon storage, maintain water quality and support northern biodiversity is threatened by a combination of climate change and inappropriate land management. Historical drainage and increasing temperatures threaten the maintenance of the high water tables required for effective peatland functioning, and there is an urgent need to develop appropriate adaptation strategies. Here we use a large-scale replicated experimental design to test the effects of artificial drainage and drain blocking upon soil moisture and cranefly (Diptera: Tipulidae) abundance. Craneflies constitute a key component of peatland biological communities; they are important herbivores and a major prey item for breeding birds. However, they are also susceptible to drought, so are at risk from future climate change. We found that cranefly abundance increased with soil moisture, in a wedge-shaped relationship; high soil moisture is a necessary condition for high cranefly abundance. Blocking drains increased both soil moisture (by 0.06 m 3  m −3 in 2009 and 0.23 m 3  m −3 in 2010) and cranefly abundance (1.3-fold in 2009, 4.5-fold in 2010), but the strength and significance of the effects varied between years. The benefits of restoring ecosystem moisture levels are likely to be greatest during dry years and at dry sites. This study provides some of the first evidence that adaptation management can potentially reduce some of the negative effects of climate change on vulnerable peatland systems. Management to maintain or increase soil moisture in peatlands can therefore be expected to increase populations of craneflies and their avian predators (which are of conservation and economic interest), but also increase the resilience of the ecosystem to future warming and increasingly frequent droughts, and improve carbon storage and water quality.
    Print ISSN: 1354-1013
    Electronic ISSN: 1365-2486
    Topics: Biology , Energy, Environment Protection, Nuclear Power Engineering , Geography
    Published by Wiley
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  • 3
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    Mechanisms underpinning climatic impacts on natural populations: altered species interactions are more important than direct effects (2014)
    Wiley
    Details
    Publication Date: 2014-03-29
    Description: Shifts in species' distribution and abundance in response to climate change have been well documented, but the underpinning processes are still poorly understood. We present the results of a systematic literature review and meta-analysis investigating the frequency and importance of different mechanisms by which climate has impacted natural populations. Most studies were from temperate latitudes of North America and Europe; almost half investigated bird populations. We found significantly greater support for indirect, biotic mechanisms than direct, abiotic mechanisms as mediators of the impact of climate on populations. In addition, biotic effects tended to have greater support than abiotic factors in studies of species from higher trophic levels. For primary consumers, the impact of climate was equally mediated by biotic and abiotic mechanisms, whereas for higher level consumers the mechanisms were most frequently biotic, such as predation or food availability. Biotic mechanisms were more frequently supported in studies that reported a directional trend in climate than in studies with no such climatic change, although sample sizes for this comparison were small. We call for more mechanistic studies of climate change impacts on populations, particularly in tropical systems.
    Print ISSN: 1354-1013
    Electronic ISSN: 1365-2486
    Topics: Biology , Energy, Environment Protection, Nuclear Power Engineering , Geography
    Published by Wiley
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  • 4
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    Impaired B and T cell antigen receptor signaling in p110delta PI 3-kinase mutant mice (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-20
    Description: Class IA phosphoinositide 3-kinases (PI3Ks) are a family of p85/p110 heterodimeric lipid kinases that generate second messenger signals downstream of tyrosine kinases, thereby controlling cell metabolism, growth, proliferation, differentiation, motility, and survival. Mammals express three class IA catalytic subunits: p110alpha, p110beta, and p110delta. It is unclear to what extent these p110 isoforms have overlapping or distinct biological roles. Mice expressing a catalytically inactive form of p110delta (p110delta(D910A)) were generated by gene targeting. Antigen receptor signaling in B and T cells was impaired and immune responses in vivo were attenuated in p110delta mutant mice. They also developed inflammatory bowel disease. These results reveal a selective role for p110delta in immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okkenhaug, Klaus -- Bilancio, Antonio -- Farjot, Geraldine -- Priddle, Helen -- Sancho, Sara -- Peskett, Emma -- Pearce, Wayne -- Meek, Stephen E -- Salpekar, Ashreena -- Waterfield, Michael D -- Smith, Andrew J H -- Vanhaesebroeck, Bart -- New York, N.Y. -- Science. 2002 Aug 9;297(5583):1031-4. Epub 2002 Jul 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, 91 Riding House Street, London W1W 7BS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12130661" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; B-Lymphocytes/enzymology/*immunology ; Bone Marrow Cells/cytology ; Catalytic Domain ; Cell Differentiation ; Cell Division ; Female ; Gene Targeting ; Hematopoietic Stem Cells/cytology ; Immunoglobulins/blood ; Inflammatory Bowel Diseases/immunology/pathology ; Interleukin-2/biosynthesis ; Intestinal Mucosa/pathology ; Lymph Nodes/cytology/pathology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Phosphatidylinositol 3-Kinases/genetics/*metabolism ; Point Mutation ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Receptors, Antigen, B-Cell/*metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Signal Transduction ; Spleen/cytology/pathology ; T-Lymphocytes/enzymology/*immunology ; Thymus Gland/cytology
    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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    Angiogenesis selectively requires the p110alpha isoform of PI3K to control endothelial cell migration (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-05-02
    Description: Phosphoinositide 3-kinases (PI3Ks) signal downstream of multiple cell-surface receptor types. Class IA PI3K isoforms couple to tyrosine kinases and consist of a p110 catalytic subunit (p110alpha, p110beta or p110delta), constitutively bound to one of five distinct p85 regulatory subunits. PI3Ks have been implicated in angiogenesis, but little is known about potential selectivity among the PI3K isoforms and their mechanism of action in endothelial cells during angiogenesis in vivo. Here we show that only p110alpha activity is essential for vascular development. Ubiquitous or endothelial cell-specific inactivation of p110alpha led to embryonic lethality at mid-gestation because of severe defects in angiogenic sprouting and vascular remodelling. p110alpha exerts this critical endothelial cell-autonomous function by regulating endothelial cell migration through the small GTPase RhoA. p110alpha activity is particularly high in endothelial cells and preferentially induced by tyrosine kinase ligands (such as vascular endothelial growth factor (VEGF)-A). In contrast, p110beta in endothelial cells signals downstream of G-protein-coupled receptor (GPCR) ligands such as SDF-1alpha, whereas p110delta is expressed at low level and contributes only minimally to PI3K activity in endothelial cells. These results provide the first in vivo evidence for p110-isoform selectivity in endothelial PI3K signalling during angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graupera, Mariona -- Guillermet-Guibert, Julie -- Foukas, Lazaros C -- Phng, Li-Kun -- Cain, Robert J -- Salpekar, Ashreena -- Pearce, Wayne -- Meek, Stephen -- Millan, Jaime -- Cutillas, Pedro R -- Smith, Andrew J H -- Ridley, Anne J -- Ruhrberg, Christiana -- Gerhardt, Holger -- Vanhaesebroeck, Bart -- BB/C505659/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/C505659/2/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0601093/Medical Research Council/United Kingdom -- G0601093(79633)/Medical Research Council/United Kingdom -- G0700711/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2008 May 29;453(7195):662-6. doi: 10.1038/nature06892. Epub 2008 Apr 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Cell Signalling, Institute of Cancer, Queen Mary, University of London, Charterhouse Square, London EC1M 6BQ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18449193" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Movement ; Cells, Cultured ; Class I Phosphatidylinositol 3-Kinases ; Endothelial Cells/*cytology/*enzymology ; Female ; Humans ; Mice ; *Neovascularization, Physiologic ; Phosphatidylinositol 3-Kinases/genetics/*metabolism ; RNA Interference ; Rats ; Signal Transduction/drug effects ; Vascular Endothelial Growth Factor A/pharmacology ; Wounds and Injuries ; rho GTP-Binding Proteins/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    Amateur scientists: Citizen projects can minimize conflicts (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pearce-Higgins, James W -- England -- Nature. 2015 Sep 24;525(7570):455. doi: 10.1038/525455b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉British Trust for Ornithology, Thetford, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26399822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds ; *Conflict of Interest ; Cost-Benefit Analysis ; Data Collection ; Great Britain ; *Hobbies ; Motivation ; *Research Design ; Science/*manpower ; *Volunteers/psychology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
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    Spatial and habitat variation in aphid, butterfly, moth and bird phenologies over the last half century (2019)
    Wiley
    Details
    Publication Date: 2019
    Description: Abstract Global warming has advanced the timing of biological events, potentially leading to disruption across trophic levels. The potential importance of phenological change as a driver of population trends has been suggested. To fully understand possible impacts, there is a need to quantify the scale of these changes spatially and according to habitat type. We studied the relationship between phenological trends, space and habitat type between 1965 to 2012 using an extensive UK dataset comprising 269 aphid, bird, butterfly and moth species. We modelled phenologies using generalized additive mixed models that included covariates for geographical (latitude, longitude, altitude), temporal (year, season) and habitat terms (woodland, scrub, grassland). Model selection showed that a baseline model with geographical and temporal components explained the variation in phenologies better than either a model in which space and time interacted or a habitat model without spatial terms. This baseline model showed strongly that phenologies shifted progressively earlier over time, that increasing altitude produced later phenologies and that a strong spatial component determined phenological timings, particularly latitude. The seasonal timing of a phenological event, in terms of whether it fell in the first or second half of the year, did not result in substantially different trends for butterflies. For moths, early season phenologies advanced more rapidly than those recorded later. Whilst temporal trends across all habitats resulted in earlier phenologies over time, agricultural habitats produced significantly later phenologies than most other habitats studied, probably because of non‐climatic drivers. A model with a significant habitat‐time interaction was the best‐fitting model for birds, moths and butterflies, emphasising that the rates of phenological advance also differ among habitats for these groups. Our results suggest the presence of strong spatial gradients in mean seasonal timing, and non‐linear trends towards earlier seasonal timing that varies in form and rate among habitat types. This article is protected by copyright. All rights reserved.
    Print ISSN: 1354-1013
    Electronic ISSN: 1365-2486
    Topics: Biology , Energy, Environment Protection, Nuclear Power Engineering , Geography
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  • 8
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    Passerines may be sufficiently plastic to track temperature-mediated shifts in optimum lay date (2016)
    Wiley
    Details
    Publication Date: 2016-05-14
    Description: Projecting the fates of populations under climate change is one of global change biology's foremost challenges. Here, we seek to identify the contributions that temperature-mediated local adaptation and plasticity make to spatial variation in nesting phenology, a phenotypic trait showing strong responses to warming. We apply a mixed modeling framework to a Britain-wide spatiotemporal dataset comprising 〉100 000 records of first egg dates from four single-brooded passerine bird species. The average temperature during a specific time period (sliding window) strongly predicts spatiotemporal variation in lay date. All four species exhibit phenological plasticity, advancing lay date by 2–5 days °C −1 . The initiation of this sliding window is delayed further north, which may be a response to a photoperiod threshold. Using clinal trends in phenology and temperature, we are able to estimate the temperature sensitivity of selection on lay date ( B ), but our estimates are highly sensitive to the temporal position of the sliding window. If the sliding window is of fixed duration with a start date determined by photoperiod, we find B is tracked by phenotypic plasticity. If, instead, we allow the start and duration of the sliding window to change with latitude, we find plasticity does not track B , although in this case, at odds with theoretical expectations, our estimates of B differ across latitude vs. longitude. We argue that a model combining photoperiod and mean temperature is most consistent with current understanding of phenological cues in passerines, the results from which suggest that each species could respond to projected increases in spring temperatures through plasticity alone. However, our estimates of B require further validation.
    Print ISSN: 1354-1013
    Electronic ISSN: 1365-2486
    Topics: Biology , Energy, Environment Protection, Nuclear Power Engineering , Geography
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  • 9
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    Inactivation of PI(3)K p110delta breaks regulatory T-cell-mediated immune tolerance to cancer (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-06-12
    Description: Inhibitors against the p110delta isoform of phosphoinositide-3-OH kinase (PI(3)K) have shown remarkable therapeutic efficacy in some human leukaemias. As p110delta is primarily expressed in leukocytes, drugs against p110delta have not been considered for the treatment of solid tumours. Here we report that p110delta inactivation in mice protects against a broad range of cancers, including non-haematological solid tumours. We demonstrate that p110delta inactivation in regulatory T cells unleashes CD8(+) cytotoxic T cells and induces tumour regression. Thus, p110delta inhibitors can break tumour-induced immune tolerance and should be considered for wider use in oncology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4501086/" 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/PMC4501086/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ali, Khaled -- Soond, Dalya R -- Pineiro, Roberto -- Hagemann, Thorsten -- Pearce, Wayne -- Lim, Ee Lyn -- Bouabe, Hicham -- Scudamore, Cheryl L -- Hancox, Timothy -- Maecker, Heather -- Friedman, Lori -- Turner, Martin -- Okkenhaug, Klaus -- Vanhaesebroeck, Bart -- 095691/Wellcome Trust/United Kingdom -- 095691/Z/11/Z/Wellcome Trust/United Kingdom -- 12888/Cancer Research UK/United Kingdom -- 14355/Cancer Research UK/United Kingdom -- A10200/Cancer Research UK/United Kingdom -- A12888/Cancer Research UK/United Kingdom -- A15965/Cancer Research UK/United Kingdom -- BB/E009867/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- C18270/A12888/Cancer Research UK/United Kingdom -- C23338/A10200/Cancer Research UK/United Kingdom -- C23338/A15965/Cancer Research UK/United Kingdom -- England -- Nature. 2014 Jun 19;510(7505):407-11. doi: 10.1038/nature13444. Epub 2014 Jun 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] UCL Cancer Institute, Paul O'Gorman Building, University College London, 72 Huntley Street London WC1E 6DD, UK [2]. ; 1] Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK [2] [3]. ; Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. ; UCL Cancer Institute, Paul O'Gorman Building, University College London, 72 Huntley Street London WC1E 6DD, UK. ; Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK. ; Mary Lyon Centre, MRC Harwell, Harwell Science and Innovation Campus, Harwell OX11 0RD, UK. ; Piramed Pharma, 957 Buckingham Avenue, Slough, Berkshire SL1 4NL, UK. ; Cancer Signaling and Translational Oncology, Genentech Inc, 1 DNA Way, South San Francisco, California 94080-4990, USA. ; 1] Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24919154" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/pharmacology ; Enzyme Activation/drug effects ; Enzyme Inhibitors/*pharmacology ; Immune Tolerance/*drug effects/immunology ; Mice ; Neoplasms/*enzymology/*immunology ; Phosphatidylinositol 3-Kinases/*metabolism ; T-Lymphocytes, Regulatory/*drug effects/enzymology/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
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    Transparency: issues are not that simple (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-03-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pearce, Warren -- Hartley, Sarah -- Nerlich, Brigitte -- England -- Nature. 2016 Mar 3;531(7592):35. doi: 10.1038/531035d.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Nottingham, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26935688" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; *Information Dissemination ; Research/*standards
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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