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  • Wiley  (11)
  • International Union of Crystallography (IUC)  (7)
  • Nature Publishing Group (NPG)  (4)
  • Cambridge University Press
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  • 1
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    Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-04-11
    Description: In obesity and type 2 diabetes, Glut4 glucose transporter expression is decreased selectively in adipocytes. Adipose-specific knockout or overexpression of Glut4 alters systemic insulin sensitivity. Here we show, using DNA array analyses, that nicotinamide N-methyltransferase (Nnmt) is the most strongly reciprocally regulated gene when comparing gene expression in white adipose tissue (WAT) from adipose-specific Glut4-knockout or adipose-specific Glut4-overexpressing mice with their respective controls. NNMT methylates nicotinamide (vitamin B3) using S-adenosylmethionine (SAM) as a methyl donor. Nicotinamide is a precursor of NAD(+), an important cofactor linking cellular redox states with energy metabolism. SAM provides propylamine for polyamine biosynthesis and donates a methyl group for histone methylation. Polyamine flux including synthesis, catabolism and excretion, is controlled by the rate-limiting enzymes ornithine decarboxylase (ODC) and spermidine-spermine N(1)-acetyltransferase (SSAT; encoded by Sat1) and by polyamine oxidase (PAO), and has a major role in energy metabolism. We report that NNMT expression is increased in WAT and liver of obese and diabetic mice. Nnmt knockdown in WAT and liver protects against diet-induced obesity by augmenting cellular energy expenditure. NNMT inhibition increases adipose SAM and NAD(+) levels and upregulates ODC and SSAT activity as well as expression, owing to the effects of NNMT on histone H3 lysine 4 methylation in adipose tissue. Direct evidence for increased polyamine flux resulting from NNMT inhibition includes elevated urinary excretion and adipocyte secretion of diacetylspermine, a product of polyamine metabolism. NNMT inhibition in adipocytes increases oxygen consumption in an ODC-, SSAT- and PAO-dependent manner. Thus, NNMT is a novel regulator of histone methylation, polyamine flux and NAD(+)-dependent SIRT1 signalling, and is a unique and attractive target for treating obesity and type 2 diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4107212/" 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/PMC4107212/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kraus, Daniel -- Yang, Qin -- Kong, Dong -- Banks, Alexander S -- Zhang, Lin -- Rodgers, Joseph T -- Pirinen, Eija -- Pulinilkunnil, Thomas C -- Gong, Fengying -- Wang, Ya-chin -- Cen, Yana -- Sauve, Anthony A -- Asara, John M -- Peroni, Odile D -- Monia, Brett P -- Bhanot, Sanjay -- Alhonen, Leena -- Puigserver, Pere -- Kahn, Barbara B -- K01 DK094943/DK/NIDDK NIH HHS/ -- K08 DK090149/DK/NIDDK NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- P01CA120964/CA/NCI NIH HHS/ -- P30 DK040561/DK/NIDDK NIH HHS/ -- P30 DK0460200/DK/NIDDK NIH HHS/ -- P30 DK046200/DK/NIDDK NIH HHS/ -- P30 DK057521/DK/NIDDK NIH HHS/ -- P30 DK57521/DK/NIDDK NIH HHS/ -- P30CA006516-46/CA/NCI NIH HHS/ -- R01 DK069966/DK/NIDDK NIH HHS/ -- R01 DK100385/DK/NIDDK NIH HHS/ -- R01 DK69966/DK/NIDDK NIH HHS/ -- R37 DK043051/DK/NIDDK NIH HHS/ -- R37 DK43051/DK/NIDDK NIH HHS/ -- England -- Nature. 2014 Apr 10;508(7495):258-62. doi: 10.1038/nature13198.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA [2] [3] Division of Nephrology, Department of Internal Medicine I, Wurzburg University Hospital, Oberdurrbacher Strasse 6, 97080 Wurzburg, Germany (D.K.); Department of Medicine, Physiology and Biophysics, Center for Diabetes Research and Treatment, and Center for Epigenetics and Metabolism, University of California, Irvine, California 92697, USA (Q.Y.); Research Programs Unit, Molecular Neurology, Biomedicum Helsinki, University of Helsinki, 00290, Helsinki, Finland (E.P.); Department of Biochemistry and Molecular Biology, Faculty of Medicine, Dalhousie Medicine New Brunswick, Dalhousie University, Saint John, New Brunswick E2L4L5, USA (T.C.P.); Department of Endocrinology, Key Laboratory of Endocrinology of Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China (F.G.); School of Pharmacy, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland (L.A.). ; Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA. ; Department of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Biotechnology and Molecular Medicine, A.I. Virtanen Institute for Molecular Sciences, Biocenter Kuopio, University of Eastern Finland, Kuopio Campus, PO Box 1627, FI-70211 Kuopio, Finland [2] Division of Nephrology, Department of Internal Medicine I, Wurzburg University Hospital, Oberdurrbacher Strasse 6, 97080 Wurzburg, Germany (D.K.); Department of Medicine, Physiology and Biophysics, Center for Diabetes Research and Treatment, and Center for Epigenetics and Metabolism, University of California, Irvine, California 92697, USA (Q.Y.); Research Programs Unit, Molecular Neurology, Biomedicum Helsinki, University of Helsinki, 00290, Helsinki, Finland (E.P.); Department of Biochemistry and Molecular Biology, Faculty of Medicine, Dalhousie Medicine New Brunswick, Dalhousie University, Saint John, New Brunswick E2L4L5, USA (T.C.P.); Department of Endocrinology, Key Laboratory of Endocrinology of Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China (F.G.); School of Pharmacy, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland (L.A.). ; 1] Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA [2] Division of Nephrology, Department of Internal Medicine I, Wurzburg University Hospital, Oberdurrbacher Strasse 6, 97080 Wurzburg, Germany (D.K.); Department of Medicine, Physiology and Biophysics, Center for Diabetes Research and Treatment, and Center for Epigenetics and Metabolism, University of California, Irvine, California 92697, USA (Q.Y.); Research Programs Unit, Molecular Neurology, Biomedicum Helsinki, University of Helsinki, 00290, Helsinki, Finland (E.P.); Department of Biochemistry and Molecular Biology, Faculty of Medicine, Dalhousie Medicine New Brunswick, Dalhousie University, Saint John, New Brunswick E2L4L5, USA (T.C.P.); Department of Endocrinology, Key Laboratory of Endocrinology of Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China (F.G.); School of Pharmacy, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland (L.A.). ; Department of Pharmacology, Weill Medical College of Cornell University, 1300 York Avenue, New York, New York 10065, USA. ; Division of Signal Transduction, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Ave, Boston, Massachusetts 02215, USA. ; Isis Pharmaceuticals, 1896 Rutherford Road, Carlsbad, California 92008-7326, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24717514" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/metabolism ; Adipocytes/metabolism/secretion ; Adipose Tissue/enzymology/metabolism ; Adipose Tissue, White/enzymology/metabolism ; Animals ; Diabetes Mellitus, Type 2/enzymology/metabolism ; *Diet ; Energy Metabolism ; Fatty Liver ; Gene Knockdown Techniques ; Glucose Intolerance ; Glucose Transporter Type 4/deficiency/genetics/metabolism ; Insulin Resistance ; Liver/enzymology ; Male ; Mice ; Mice, Inbred C57BL ; NAD/metabolism ; Niacinamide/metabolism ; Nicotinamide N-Methyltransferase/*deficiency/genetics/*metabolism ; Obesity/*enzymology/etiology/genetics/*prevention & control ; Ornithine Decarboxylase/metabolism ; Oxidoreductases Acting on CH-NH Group Donors/metabolism ; S-Adenosylmethionine/metabolism ; Sirtuin 1/metabolism ; Spermine/analogs & derivatives/metabolism ; Thinness/enzymology/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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  • 2
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    Differential positioning of adherens junctions is associated with initiation of epithelial folding (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-03-30
    Description: During tissue morphogenesis, simple epithelial sheets undergo folding to form complex structures. The prevailing model underlying epithelial folding involves cell shape changes driven by myosin-dependent apical constriction. Here we describe an alternative mechanism that requires differential positioning of adherens junctions controlled by modulation of epithelial apical-basal polarity. Using live embryo imaging, we show that before the initiation of dorsal transverse folds during Drosophila gastrulation, adherens junctions shift basally in the initiating cells, but maintain their original subapical positioning in the neighbouring cells. Junctional positioning in the dorsal epithelium depends on the polarity proteins Bazooka and Par-1. In particular, the basal shift that occurs in the initiating cells is associated with a progressive decrease in Par-1 levels. We show that uniform reduction of the activity of Bazooka or Par-1 results in uniform apical or lateral positioning of junctions and in each case dorsal fold initiation is abolished. In addition, an increase in the Bazooka/Par-1 ratio causes formation of ectopic dorsal folds. The basal shift of junctions not only alters the apical shape of the initiating cells, but also forces the lateral membrane of the adjacent cells to bend towards the initiating cells, thereby facilitating tissue deformation. Our data thus establish a direct link between modification of epithelial polarity and initiation of epithelial folding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597240/" 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/PMC3597240/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Yu-Chiun -- Khan, Zia -- Kaschube, Matthias -- Wieschaus, Eric F -- 5R37HD15587/HD/NICHD NIH HHS/ -- P50 GM071508/GM/NIGMS NIH HHS/ -- R37 HD015587/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Mar 28;484(7394):390-3. doi: 10.1038/nature10938.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22456706" target="_blank"〉PubMed〈/a〉
    Keywords: Adherens Junctions/*physiology/ultrastructure ; Animals ; *Cell Polarity ; Cell Shape ; Choristoma ; Drosophila Proteins/deficiency/genetics/metabolism ; Drosophila melanogaster/*cytology/*embryology/genetics/metabolism ; Epithelial Cells/*cytology/metabolism/ultrastructure ; Epithelium/*embryology/metabolism/ultrastructure ; Gastrula/cytology/embryology/metabolism/ultrastructure ; Gastrulation/*physiology ; Glycogen Synthase Kinase 3 ; Intracellular Signaling Peptides and Proteins/deficiency/genetics/metabolism ; Protein-Serine-Threonine Kinases/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    The amino acid sensor GCN2 controls gut inflammation by inhibiting inflammasome activation (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-03-17
    Description: The integrated stress response (ISR) is a homeostatic mechanism by which eukaryotic cells sense and respond to stress-inducing signals, such as amino acid starvation. General controlled non-repressed (GCN2) kinase is a key orchestrator of the ISR, and modulates protein synthesis in response to amino acid starvation. Here we demonstrate in mice that GCN2 controls intestinal inflammation by suppressing inflammasome activation. Enhanced activation of ISR was observed in intestinal antigen presenting cells (APCs) and epithelial cells during amino acid starvation, or intestinal inflammation. Genetic deletion of Gcn2 (also known as Eif2ka4) in CD11c(+) APCs or intestinal epithelial cells resulted in enhanced intestinal inflammation and T helper 17 cell (TH17) responses, owing to enhanced inflammasome activation and interleukin (IL)-1beta production. This was caused by reduced autophagy in Gcn2(-/-) intestinal APCs and epithelial cells, leading to increased reactive oxygen species (ROS), a potent activator of inflammasomes. Thus, conditional ablation of Atg5 or Atg7 in intestinal APCs resulted in enhanced ROS and TH17 responses. Furthermore, in vivo blockade of ROS and IL-1beta resulted in inhibition of TH17 responses and reduced inflammation in Gcn2(-/-) mice. Importantly, acute amino acid starvation suppressed intestinal inflammation via a mechanism dependent on GCN2. These results reveal a mechanism that couples amino acid sensing with control of intestinal inflammation via GCN2.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4854628/" 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/PMC4854628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ravindran, Rajesh -- Loebbermann, Jens -- Nakaya, Helder I -- Khan, Nooruddin -- Ma, Hualing -- Gama, Leonardo -- Machiah, Deepa K -- Lawson, Benton -- Hakimpour, Paul -- Wang, Yi-chong -- Li, Shuzhao -- Sharma, Prachi -- Kaufman, Randal J -- Martinez, Jennifer -- Pulendran, Bali -- R01 DK088227/DK/NIDDK NIH HHS/ -- R01 DK103185/DK/NIDDK NIH HHS/ -- R37 AI048638/AI/NIAID NIH HHS/ -- R37 DK042394/DK/NIDDK NIH HHS/ -- R37 DK057665/DK/NIDDK NIH HHS/ -- U19 AI057266/AI/NIAID NIH HHS/ -- U19 AI090023/AI/NIAID NIH HHS/ -- ZIA ES103286-01/Intramural NIH HHS/ -- England -- Nature. 2016 Mar 24;531(7595):523-7. doi: 10.1038/nature17186. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center, Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. ; School of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo 05508, Brazil. ; Department of Biotechnology and Bioinformatics, School of Life Sciences, University of Hyderabad, Hyderabad 500 046, India. ; Division of Pathology, Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. ; Virology Core, Emory Vaccine Center and Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. ; Degenerative Disease Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037 USA. ; National Institute of Environmental Health Sciences, Mail Drop D2-01 Research Triangle Park, North Carolina 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982722" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/administration & dosage/deficiency/*metabolism/pharmacology ; Animals ; Antigen-Presenting Cells/immunology/metabolism ; Autophagy ; Colitis/etiology/*metabolism/pathology/prevention & control ; Disease Models, Animal ; Epithelial Cells/metabolism ; Female ; Humans ; Inflammasomes/*antagonists & inhibitors/metabolism ; Inflammation/etiology/*metabolism/pathology/prevention & control ; Interleukin-1beta/immunology ; Intestines/*metabolism/*pathology ; Male ; Mice ; Microtubule-Associated Proteins/deficiency/metabolism ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Reactive Oxygen Species/metabolism ; Stress, Physiological ; Th17 Cells/immunology ; Ubiquitin-Activating Enzymes/deficiency/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    A receptor heteromer mediates the male perception of female attractants in plants (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-02-11
    Description: Sexual reproduction requires recognition between the male and female gametes. In flowering plants, the immobile sperms are delivered to the ovule-enclosed female gametophyte by guided pollen tube growth. Although the female gametophyte-secreted peptides have been identified to be the chemotactic attractant to the pollen tube, the male receptor(s) is still unknown. Here we identify a cell-surface receptor heteromer, MDIS1-MIK, on the pollen tube that perceives female attractant LURE1 in Arabidopsis thaliana. MDIS1, MIK1 and MIK2 are plasma-membrane-localized receptor-like kinases with extracellular leucine-rich repeats and an intracellular kinase domain. LURE1 specifically binds the extracellular domains of MDIS1, MIK1 and MIK2, whereas mdis1 and mik1 mik2 mutant pollen tubes respond less sensitively to LURE1. Furthermore, LURE1 triggers dimerization of the receptors and activates the kinase activity of MIK1. Importantly, transformation of AtMDIS1 to the sister species Capsella rubella can partially break down the reproductive isolation barrier. Our findings reveal a new mechanism of the male perception of the female attracting signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Tong -- Liang, Liang -- Xue, Yong -- Jia, Peng-Fei -- Chen, Wei -- Zhang, Meng-Xia -- Wang, Ying-Chun -- Li, Hong-Ju -- Yang, Wei-Cai -- England -- Nature. 2016 Mar 10;531(7593):241-4. doi: 10.1038/nature16975. Epub 2016 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China. ; University of Chinese Academy of Sciences, Beijing 100049, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863186" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/*metabolism/physiology ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Capsella/genetics/metabolism/physiology ; Cell Membrane/metabolism ; Mutation ; Ovule/metabolism ; Phenotype ; Phosphotransferases/chemistry/genetics/*metabolism ; Pollen Tube/genetics/growth & development/metabolism ; Protein Kinases/genetics/metabolism ; Protein Multimerization ; Protein Structure, Quaternary ; Protein Structure, Tertiary ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Reproduction ; *Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Introduction to CAUSES: Description of weather and climate models and their near-surface temperature errors in 5-day hindcasts near the Southern Great Plains (2018)
    Wiley
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    Publication Date: 2018-02-17
    Description: We introduce the Clouds Above the United States and Errors at the Surface (CAUSES) project with its aim of better understanding the physical processes leading to warm screen-temperature biases over the American Midwest in many numerical models. In this first of four companion papers, 11 different models, from 9 institutes, perform a series of 5-day hindcasts, each initialised from reanalyses. After describing the common experimental protocol and detailing each model configuration, a gridded temperature data set is derived from observations and used to show that all the models have a warm bias over parts of the Midwest. Additionally, a strong diurnal cycle in the screen-temperature bias is found in most models. In some models the bias is largest around midday, while in others it is largest during the night. At the Department of Energy Atmospheric Radiation Measurement Southern Great Plains (SGP) site, the model biases are shown to extend several kilometers into the atmosphere. Finally, to provide context for the companion papers, in which observations from the SGP site are used to evaluate the different processes contributing to errors there, it is shown that there are numerous locations across the Midwest where the diurnal cycle of the error is highly correlated with the diurnal cycle of the error at SGP. This suggests that conclusions drawn from detailed evaluation of models using instruments located at SGP will be representative of errors that are prevalent over a larger spatial scale.
    Print ISSN: 0148-0227
    Topics: Geosciences , Physics
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  • 6
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    CAUSES: Attribution of Surface Radiation Biases in NWP and Climate Models near the U.S. Southern Great Plains (2018)
    Wiley
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    Publication Date: 2018-03-06
    Description: Many numerical weather prediction and climate models exhibit too warm lower tropospheres near the mid-latitude continents. The warm bias has been shown to coincide with important surface radiation biases that likely play a critical role in the inception or the growth of the warm bias. This paper presents an attribution study on the net radiation biases in 9 model simulations, performed in the framework of the CAUSES project (Clouds Above the United States and Errors at the Surface). Contributions from deficiencies in the surface properties, clouds, water vapor and aerosols are quantified, using an array of radiation measurement stations near the ARM SGP site. Furthermore, an in-depth analysis is shown to attribute the radiation errors to specific cloud regimes. The net surface shortwave radiation is overestimated in all models throughout most of the simulation period. Cloud errors are shown to contribute most to this overestimation, although non-negligible contributions from the surface albedo exist in most models. Missing deep cloud events and/or simulating deep clouds with too weak cloud-radiative effects dominate in the cloud-related radiation errors. Some models have compensating errors between excessive occurrence of deep cloud, but largely underestimating their radiative effect, while other models miss deep cloud events altogether. Surprisingly, even the latter models tend to produce too much and too frequent afternoon surface precipitation. This suggests that rather than issues with the triggering of deep convection, cloud-radiative deficiencies are related to too weak convective cloud detrainment and too large precipitation efficiencies.
    Print ISSN: 0148-0227
    Topics: Geosciences , Physics
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  • 7
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    CAUSES: On the role of surface energy budget errors to the warm surface air temperature error over the Central U.S. (2018)
    Wiley
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    Publication Date: 2018-02-28
    Description: Many weather forecast and climate models simulate warm surface air temperature (T 2m ) biases over mid-latitude continents during the summertime, especially over the Great Plains. We present here one of a series of papers from a multi-model intercomparison project (CAUSES: Cloud Above the United States and Errors at the Surface), which aims to evaluate the role of cloud, radiation, and precipitation biases in contributing to the T 2m bias using a short-term hindcast approach during the spring and summer of 2011. Observations are mainly from the Atmospheric Radiation Measurement (ARM) Southern Great Plains (SGP) sites. The present study examines the contributions of surface energy budget errors. All participating models simulate too much net shortwave and longwave fluxes at the surface but with no consistent mean bias sign in turbulent fluxes over the Central U.S. and SGP. Nevertheless, biases in the net shortwave and downward longwave fluxes, as well as surface evaporative fraction (EF) are contributors to T 2m bias. Radiation biases are largely affected by cloud simulations, while EF bias is largely affected by soil moisture modulated by seasonal accumulated precipitation and evaporation. An approximate equation based upon the surface energy budget is derived to further quantify the magnitudes of radiation and EF contributions to T 2m bias. Our analysis ascribes that a large EF underestimate is the dominant source of error in all models with a large positive temperature bias, whereas an EF overestimate compensates for an excess of absorbed shortwave radiation in nearly all the models with the smallest temperature bias.
    Print ISSN: 0148-0227
    Topics: Geosciences , Physics
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  • 8
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    Simulations of observed auroral brightening caused by solar wind dynamic pressure enhancements under different interplanetary magnetic field conditions (2011)
    Wiley
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    Publication Date: 2011-06-28
    Description: Solar wind dynamic pressure (Pdyn) enhancements have been observed to cause large-scale auroral brightening. The mechanism for this kind of auroral brightening is still a topic of current space research. Using the global piecewise parabolic method Lagrangian remap (PPMLR)-MHD simulation model, we investigate three auroral brightening events caused by dynamic pressure enhancement under different interplanetary magnetic field (IMF) conditions: (1) Bz 〈 0 and By 〉 0 on 11 August 2000, (2) Bz 〈 0 and By 〈 0 on 8 May 2001, and (3) Bz ≥ 0 on 21 January 2005. We show that the auroral location depends on the IMF conditions. Under southward IMF conditions, when By is negative, the duskside aurora is located more equatorward at around 70° magnetic latitude (MLAT) for all magnetic local times; when By is positive, the duskside aurora can even reach beyond 80° MLAT. A smaller and more localized response is seen when the IMF Bz is nearly zero or northward, as shown in previous studies. Our simulation results are consistent with these observations, indicating that the observed aurora activities could be caused by solar wind dynamic pressure enhancements. The simulation results suggest that the enhancement of Pdyn can increase the ionospheric transpolar potential and the corresponding field-aligned currents, leading to the observed auroral brightening.
    Print ISSN: 0148-0227
    Topics: Geosciences , Physics
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  • 9
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    trans-Tetrakis[N-(adamantan-1-yl)pyridine-4-carboxamide]dichloridomanganese(II)–N-(adamantan-1-yl)pyridine-4-carboxamide (1/2) (2012)
    International Union of Crystallography (IUC)
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    Publication Date: 2012-03-15
    Description: The asymmetric unit of the title compound, [MnCl2(C16H20N2O)4]·2C16H20N2O, is composed of two coordinating N-(adamantan-1-yl)pyridine-4-carboxamide molecules, one Cl− anion, an MnII ion, lying on an inversion centre, and one free N-(adamantan-1-yl)pyridine-4-carboxamide molecule. The distorted octahedral Mn environment comprises two terminal Cl atoms and four monodentate N atoms from four organic ligands. All the carbamoyl N atoms are involved in intermolecular N—H...O hydrogen-bonding interactions which link the molecules into a chain along the a axis.
    Electronic ISSN: 1600-5368
    Topics: Chemistry and Pharmacology , Geosciences
    Published by International Union of Crystallography (IUC)
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  • 10
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    4-Methylanilinium 2-carboxyacetate (2012)
    International Union of Crystallography (IUC)
    Details
    Publication Date: 2012-06-03
    Description: During the formation of the title salt, C7H10N+·C3H3O4−, an H atom of a carboxyl group was transferred to the amino group. All non-H atoms of the cation are essentially coplanar [r.m.s. deviation = 0.007 (4) Å]. The mean planes of the carboxylate and carboxyl groups of the anion form a dihedral of 69.67 (1)°. In the crystal, N—H...O and O—H...O hydrogen bonds connect the anions and cations, forming a two-dimensional network parallel to the bc plane.
    Electronic ISSN: 1600-5368
    Topics: Chemistry and Pharmacology , Geosciences
    Published by International Union of Crystallography (IUC)
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