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  • 1
    Publication Date: 2016-05-12
    Description: With 69% of the world's population predicted to live in cities by 2050, modification to local climates, in particular Urban Heat Islands, have become a well studied phenomenon. However few studies have considered how horizontal winds modify the spatial pattern in a process named Urban Heat Advection (UHA) and this is most likely due to a lack of highly spatially resolved observational data. For the first time, this study separates the two-dimensional advection-induced UHI component, including its pattern and magnitude, from the locally-heated UHI component using a unique dataset of urban canopy temperatures from 29 weather stations (3 km resolution) recorded over 20 months in Birmingham, UK. The results show that the mean contribution of UHA to the warming of areas downwind of the city can be up to 1.2 °C. Using the inverse Normalized Difference Vegetation Index as a proxy for urban fraction, an upwind distance at which the urban fraction has the strongest correlation with UHA was demonstrated to be between 4–12 km. Overall, these findings suggest that urban planning and risk management needs to additionally consider UHA. However, more fundamentally, it highlights the importance of careful interpretation of long term meteorological records taken near cities when they are used to assess global warming.
    Print ISSN: 0035-9009
    Electronic ISSN: 1477-870X
    Topics: Geography , Physics
    Published by Wiley
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  • 2
    Publication Date: 2013-09-11
    Description: The rationale of α1-antitrypsin (AAT) augmentation therapy to treat progressive emphysema in AAT-deficient patients is based on inhibition of neutrophil elastase; however, the benefit of this treatment remains unclear. Here we show that clinical grade AAT (with elastase inhibitory activity) and a recombinant form of AAT (rAAT) without anti-elastase activity...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 3
    Publication Date: 2012-11-08
    Description: The use of ancient DNA in paleopathological studies of tuberculosis has largely been restricted to confirmation of disease identifications made by skeletal analysis; few attempts at obtaining genotype data from archaeological samples have been made because of the need to perform different PCRs for each genetic locus being studied in...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 4
    Publication Date: 2013-02-12
    Description: ABSTRACT The heterogeneous nature of urban environments means that atmospheric research ideally requires a dense network of sensors to adequately resolve the local climate. With recent advances in sensor technology, a number of urban meteorological networks now exist with a range of research or operational objectives. This article reviews and assesses the current status of urban meteorological networks, by examining the fundamental scientific and logistical issues related to these networks. The article concludes by making recommendations for future deployments based on the challenges encountered by existing networks, including the need for better reporting and documentation of network characteristics, standardized approaches and guidelines, along with the need to overcome financial barriers via collaborative relationships in order to establish the long-term urban networks essential for advancing urban climate research.
    Print ISSN: 0899-8418
    Electronic ISSN: 1097-0088
    Topics: Geosciences , Physics
    Published by Wiley
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  • 5
    Publication Date: 2013-02-02
    Description: X-chromosomal dystonia parkinsonism syndrome (XDP, ‘lubag’) is associated with sequence changes within the TAF1/DYT3 multiple transcript system. Although most sequence changes are intronic, one, disease-specific single-nucleotide change 3 (DSC3), is located within an exon (d4). Transcribed exon d4 occurs as part of multiple splice variants. These variants include exons d3 and d4 spliced to exons of TAF1 , and an independent transcript composed of exons d2–d4. Location of DSC3 in exon d4 and utilization of this exon in multiple splice variants suggest an important role of DSC3 in the XDP pathogenesis. To test this hypothesis, we transfected neuroblastoma cells with four expression constructs, including exons d2–d4 [d2–d4/wild-type (wt) and d2-d4/DSC3] and d3–d4 (d3–d4/wt and d3–d4/DSC3). Expression profiling revealed a dramatic effect of DSC3 on overall gene expression. Three hundred and sixty-two genes differed between cells containing d2–d4/wt and d2–d4/DSC3. Annotation clustering revealed enrichment of genes related to vesicular transport, dopamine metabolism, synapse function, Ca 2+ metabolism and oxidative stress. Two hundred and eleven genes were differentially expressed in d3–d4/wt versus d3–d4/DSC3. Annotation clustering highlighted genes in signal transduction and cell–cell interaction. The data show an important role of physiologically occurring transcript d2–d4 in normal brain function. Interference with this role by DSC3 is a likely pathological mechanism in XDP. Disturbance of dopamine function and of Ca 2+ metabolism can explain abnormal movement; loss of protection against reactive oxygen species may account for the neurodegenerative changes in XDP. Although d3–d4 also affect genes potentially related to neurodegenerative processes, their physiologic role as splice variants of TAF1 awaits further exploration.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
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  • 6
    Publication Date: 2013-10-09
    Description: Does information play a significant role in the foundations of physics? Information is the abstraction that allows us to refer to the states of systems when we choose to ignore the systems themselves. This is only possible in very particular frameworks, like in classical or quantum theory, or more generally,...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 7
    Publication Date: 2014-11-28
    Description: Article Within microbial communities, microorganisms adopt different lifestyle strategies to use the available resources. Here, the authors use an integrated ‘multi-omic’ approach to study niche breadth (generalist versus specialist lifestyles) in oleaginous microbial assemblages from an anoxic wastewater treatment tank. Nature Communications doi: 10.1038/ncomms6603 Authors: Emilie E. L. Muller, Nicolás Pinel, Cédric C. Laczny, Michael R. Hoopmann, Shaman Narayanasamy, Laura A. Lebrun, Hugo Roume, Jake Lin, Patrick May, Nathan D. Hicks, Anna Heintz-Buschart, Linda Wampach, Cindy M. Liu, Lance B. Price, John D. Gillece, Cédric Guignard, James M. Schupp, Nikos Vlassis, Nitin S. Baliga, Robert L. Moritz, Paul S. Keim, Paul Wilmes
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 8
    Publication Date: 2011-02-11
    Description: Telomere dysfunction activates p53-mediated cellular growth arrest, senescence and apoptosis to drive progressive atrophy and functional decline in high-turnover tissues. The broader adverse impact of telomere dysfunction across many tissues including more quiescent systems prompted transcriptomic network analyses to identify common mechanisms operative in haematopoietic stem cells, heart and liver. These unbiased studies revealed profound repression of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha and beta (PGC-1alpha and PGC-1beta, also known as Ppargc1a and Ppargc1b, respectively) and the downstream network in mice null for either telomerase reverse transcriptase (Tert) or telomerase RNA component (Terc) genes. Consistent with PGCs as master regulators of mitochondrial physiology and metabolism, telomere dysfunction is associated with impaired mitochondrial biogenesis and function, decreased gluconeogenesis, cardiomyopathy, and increased reactive oxygen species. In the setting of telomere dysfunction, enforced Tert or PGC-1alpha expression or germline deletion of p53 (also known as Trp53) substantially restores PGC network expression, mitochondrial respiration, cardiac function and gluconeogenesis. We demonstrate that telomere dysfunction activates p53 which in turn binds and represses PGC-1alpha and PGC-1beta promoters, thereby forging a direct link between telomere and mitochondrial biology. We propose that this telomere-p53-PGC axis contributes to organ and metabolic failure and to diminishing organismal fitness in the setting of telomere dysfunction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3741661/" 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/PMC3741661/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sahin, Ergun -- Colla, Simona -- Liesa, Marc -- Moslehi, Javid -- Muller, Florian L -- Guo, Mira -- Cooper, Marcus -- Kotton, Darrell -- Fabian, Attila J -- Walkey, Carl -- Maser, Richard S -- Tonon, Giovanni -- Foerster, Friedrich -- Xiong, Robert -- Wang, Y Alan -- Shukla, Sachet A -- Jaskelioff, Mariela -- Martin, Eric S -- Heffernan, Timothy P -- Protopopov, Alexei -- Ivanova, Elena -- Mahoney, John E -- Kost-Alimova, Maria -- Perry, Samuel R -- Bronson, Roderick -- Liao, Ronglih -- Mulligan, Richard -- Shirihai, Orian S -- Chin, Lynda -- DePinho, Ronald A -- P30 DK046200/DK/NIDDK NIH HHS/ -- P30DK079638/DK/NIDDK NIH HHS/ -- R01 CA084628/CA/NCI NIH HHS/ -- R01 DK035914/DK/NIDDK NIH HHS/ -- R01 DK056690/DK/NIDDK NIH HHS/ -- R01 DK063356/DK/NIDDK NIH HHS/ -- R01 DK089185/DK/NIDDK NIH HHS/ -- U24 DK-59635/DK/NIDDK NIH HHS/ -- England -- Nature. 2011 Feb 17;470(7334):359-65. doi: 10.1038/nature09787. Epub 2011 Feb 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21307849" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/biosynthesis ; Aging/metabolism/pathology ; Animals ; Cardiomyopathies/chemically induced/metabolism/pathology/physiopathology ; Cell Proliferation ; DNA, Mitochondrial/analysis ; Doxorubicin/toxicity ; Gluconeogenesis ; Hematopoietic Stem Cells/metabolism/pathology ; Liver/cytology/metabolism ; Mice ; Mitochondria/*metabolism/*pathology ; Myocardium/cytology/metabolism ; RNA/genetics ; Reactive Oxygen Species/metabolism ; Telomerase/deficiency/genetics ; Telomere/enzymology/genetics/*metabolism/*pathology ; Transcription Factors/antagonists & inhibitors/metabolism ; Tumor Suppressor Protein p53/deficiency/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2012-08-17
    Description: Inactivation of tumour-suppressor genes by homozygous deletion is a prototypic event in the cancer genome, yet such deletions often encompass neighbouring genes. We propose that homozygous deletions in such passenger genes can expose cancer-specific therapeutic vulnerabilities when the collaterally deleted gene is a member of a functionally redundant family of genes carrying out an essential function. The glycolytic gene enolase 1 (ENO1) in the 1p36 locus is deleted in glioblastoma (GBM), which is tolerated by the expression of ENO2. Here we show that short-hairpin-RNA-mediated silencing of ENO2 selectively inhibits growth, survival and the tumorigenic potential of ENO1-deleted GBM cells, and that the enolase inhibitor phosphonoacetohydroxamate is selectively toxic to ENO1-deleted GBM cells relative to ENO1-intact GBM cells or normal astrocytes. The principle of collateral vulnerability should be applicable to other passenger-deleted genes encoding functionally redundant essential activities and provide an effective treatment strategy for cancers containing such genomic events.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3712624/" 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/PMC3712624/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, Florian L -- Colla, Simona -- Aquilanti, Elisa -- Manzo, Veronica E -- Genovese, Giannicola -- Lee, Jaclyn -- Eisenson, Daniel -- Narurkar, Rujuta -- Deng, Pingna -- Nezi, Luigi -- Lee, Michelle A -- Hu, Baoli -- Hu, Jian -- Sahin, Ergun -- Ong, Derrick -- Fletcher-Sananikone, Eliot -- Ho, Dennis -- Kwong, Lawrence -- Brennan, Cameron -- Wang, Y Alan -- Chin, Lynda -- DePinho, Ronald A -- 3 P01 CA095616-08S1/CA/NCI NIH HHS/ -- 57006984/Howard Hughes Medical Institute/ -- P01 CA095616/CA/NCI NIH HHS/ -- P01CA95616/CA/NCI NIH HHS/ -- T32-CA009361/CA/NCI NIH HHS/ -- England -- Nature. 2012 Aug 16;488(7411):337-42. doi: 10.1038/nature11331.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genomic Medicine, University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22895339" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/pharmacology/therapeutic use ; Biomarkers, Tumor/deficiency/genetics ; Brain Neoplasms/*drug therapy/*genetics/pathology ; Cell Line, Tumor ; Cell Proliferation ; Chromosomes, Human, Pair 1/genetics ; DNA-Binding Proteins/deficiency/genetics ; Enzyme Inhibitors ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Genes, Essential/*genetics ; Genes, Tumor Suppressor ; Glioblastoma/*drug therapy/*genetics/pathology ; Homozygote ; Humans ; Hydroxamic Acids/pharmacology/therapeutic use ; Mice ; Molecular Targeted Therapy/*methods ; Neoplasm Transplantation ; Phosphonoacetic Acid/analogs & derivatives/pharmacology/therapeutic use ; Phosphopyruvate Hydratase/antagonists & inhibitors/deficiency/genetics/metabolism ; RNA, Small Interfering/genetics ; Sequence Deletion/*genetics ; Tumor Suppressor Proteins/deficiency/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2014-10-25
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4346172/" 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/PMC4346172/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwarzlander, Markus -- Wagner, Stephan -- Ermakova, Yulia G -- Belousov, Vsevolod V -- Radi, Rafael -- Beckman, Joseph S -- Buettner, Garry R -- Demaurex, Nicolas -- Duchen, Michael R -- Forman, Henry J -- Fricker, Mark D -- Gems, David -- Halestrap, Andrew P -- Halliwell, Barry -- Jakob, Ursula -- Johnston, Iain G -- Jones, Nick S -- Logan, David C -- Morgan, Bruce -- Muller, Florian L -- Nicholls, David G -- Remington, S James -- Schumacker, Paul T -- Winterbourn, Christine C -- Sweetlove, Lee J -- Meyer, Andreas J -- Dick, Tobias P -- Murphy, Michael P -- 098565/Wellcome Trust/United Kingdom -- MC_U105663142/Medical Research Council/United Kingdom -- P30 CA086862/CA/NCI NIH HHS/ -- P30 ES005605/ES/NIEHS NIH HHS/ -- R01 AG027349/AG/NIA NIH HHS/ -- R01 CA169046/CA/NCI NIH HHS/ -- R01 GM073929/GM/NIGMS NIH HHS/ -- R21 AG046799/AG/NIA NIH HHS/ -- England -- Nature. 2014 Oct 23;514(7523):E12-4. doi: 10.1038/nature13858.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Crop Science and Resource Conservation (INRES), University of Bonn, Friedrich-Ebert-Allee 144, 53113 Bonn, Germany. ; Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, 117997, Russia. ; Departamento de Bioquimica, and Center for Free Radical and Biomedical Research, Facultad de Medicina, Universidad de la Republica, Avda. General Flores 2125, 11800 Montevideo, Uruguay. ; Linus Pauling Institute, Environmental Health Sciences Center, Department of Biochemistry and Biophysics, Oregon State University, Corvallis, Oregon 97331, USA. ; The University of Iowa, Department of Radiation Oncology and Interdisciplinary Graduate Program in Human Toxicology, and ESR Facility, College of Medicine, Med Labs B180K, Iowa City, Iowa 52242-1181, USA. ; Department of Cell Physiology and Metabolism, University of Geneva, 1, rue Michel-Servet, Geneva 4 CH-1211, Switzerland. ; Department of Cell and Developmental Biology and Consortium for Mitochondrial Research, University College London, Gower Street, London WC1E 6BT, UK. ; 1] Life and Environmental Sciences Unit, University of California, Merced, 5200 North Lake Road, Merced, California 95344, USA [2] Andrus Gerontology Center of the Davis School of Gerontology, University of Southern California, 3715 McClintock Avenue, Los Angeles, California 90089-0191, USA. ; Department of Plant Sciences, University of Oxford, South Parks Road, Oxford OX1 3RB, UK. ; Institute of Healthy Ageing, and Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, UK. ; School of Biochemistry and Bristol CardioVascular, University of Bristol, Medical Sciences Building, University Walk, Bristol BS8 1TD, UK. ; Department of Biochemistry, National University of Singapore, Singapore 117597, Singapore. ; Molecular, Cellular and Developmental Biology Department, University of Michigan, Ann Arbor, Michigan 48109-1048, USA. ; Department of Mathematics, South Kensington Campus, Imperial College London, London SW7 2AZ, UK. ; Universite d'Angers &INRA &Agrocampus Ouest, UMR 1345 Institut de Recherche en Horticulture et Semences, Angers, F-49045, France. ; Division of Redox Regulation, German Cancer Research Center (DKFZ), DKFZ-ZMBH Alliance, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany. ; Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. ; Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, California 94945, USA. ; Department of Physics, Institute of Molecular Biology, University of Oregon, Eugene, Oregon 97403-1229, USA. ; Department of Pediatrics, Division of Neonatology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, 60611, USA. ; Centre for Free Radical Research, Department of Pathology, University of Otago, ChristchurchPO Box 4345, Christchurch, New Zealand. ; MRC Mitochondrial Biology Unit, Hills Road, Cambridge CB2 0XY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25341790" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*metabolism ; *Longevity ; Male ; Mitochondria/*metabolism ; Superoxides/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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