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  • 1
    Publication Date: 2016-03-17
    Description: The energetic burden of continuously concentrating solutes against gradients along the tubule may render the kidney especially vulnerable to ischaemia. Acute kidney injury (AKI) affects 3% of all hospitalized patients. Here we show that the mitochondrial biogenesis regulator, PGC1alpha, is a pivotal determinant of renal recovery from injury by regulating nicotinamide adenine dinucleotide (NAD) biosynthesis. Following renal ischaemia, Pgc1alpha(-/-) (also known as Ppargc1a(-/-)) mice develop local deficiency of the NAD precursor niacinamide (NAM, also known as nicotinamide), marked fat accumulation, and failure to re-establish normal function. Notably, exogenous NAM improves local NAD levels, fat accumulation, and renal function in post-ischaemic Pgc1alpha(-/-) mice. Inducible tubular transgenic mice (iNephPGC1alpha) recapitulate the effects of NAM supplementation, including more local NAD and less fat accumulation with better renal function after ischaemia. PGC1alpha coordinately upregulates the enzymes that synthesize NAD de novo from amino acids whereas PGC1alpha deficiency or AKI attenuates the de novo pathway. NAM enhances NAD via the enzyme NAMPT and augments production of the fat breakdown product beta-hydroxybutyrate, leading to increased production of prostaglandin PGE2 (ref. 5), a secreted autacoid that maintains renal function. NAM treatment reverses established ischaemic AKI and also prevented AKI in an unrelated toxic model. Inhibition of beta-hydroxybutyrate signalling or prostaglandin production similarly abolishes PGC1alpha-dependent renoprotection. Given the importance of mitochondrial health in ageing and the function of metabolically active organs, the results implicate NAM and NAD as key effectors for achieving PGC1alpha-dependent stress resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tran, Mei T -- Zsengeller, Zsuzsanna K -- Berg, Anders H -- Khankin, Eliyahu V -- Bhasin, Manoj K -- Kim, Wondong -- Clish, Clary B -- Stillman, Isaac E -- Karumanchi, S Ananth -- Rhee, Eugene P -- Parikh, Samir M -- K08-DK090142/DK/NIDDK NIH HHS/ -- K08-DK101560/DK/NIDDK NIH HHS/ -- P30-DK079337/DK/NIDDK NIH HHS/ -- R01 DK095072/DK/NIDDK NIH HHS/ -- R01-DK095072/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 24;531(7595):528-32. doi: 10.1038/nature17184. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Nephrology and Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. ; Center for Vascular Biology Research, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. ; Division of Clinical Chemistry, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. ; Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. ; Bioinformatics and Systems Biology Core, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. ; Nephrology and Endocrine Divisions, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA. ; Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02139, USA. ; Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982719" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Hydroxybutyric Acid/metabolism ; Acute Kidney Injury/drug therapy/*metabolism ; Adipose Tissue/drug effects/metabolism ; Amino Acids/metabolism ; Animals ; Cytokines/metabolism ; Dinoprostone/biosynthesis/metabolism ; Humans ; Ischemia/drug therapy/metabolism ; Kidney/drug effects/*metabolism/physiology/physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; NAD/*biosynthesis ; Niacinamide/deficiency/pharmacology/therapeutic use ; Nicotinamide Phosphoribosyltransferase/metabolism ; Oxidation-Reduction ; Signal Transduction/drug effects ; Stress, Physiological ; Transcription Factors/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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  • 2
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Journal für Praktische Chemie/Chemiker-Zeitung 319 (1977), S. 848-856 
    ISSN: 0021-8383
    Keywords: Chemistry ; Organic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Description / Table of Contents: Physico-chemical Analysis of the Hydrolysis of N-(2-Cyanethylene-)ureaBy means of pulse-polarography, infrared and n.m.r.-spectroscopy and electronattachment-mass-spectroscopy the hydrolysis of N-(2-cyanethylene-)urea (BA 1) under relatively mild conditions has been evidenced (pH 5,6 to 9.0; T = 37° C and 22° C). With rising pH value the rate of hydrolysis increases. At pH 5.6 the hydrolysis is very slow (half life time ca. 6 days), but condensation products are already demonstrable. At pH 9.0 nearly all of BA 1 molecules are hydrolysed within 2 days under splitting of the heterocycle and formation of various hydrolysis products. On the middle pH range from 7.3 to 8.3 the formation of 2-cyanaziridine was followed and after cycle splitting various resultant products were observed. The half life time of BA 1 hydrolysis at pH 7.3 and T = 37° C has been determined to 103 ± 1 hours (0.144 m BA 1, phosphate buffer).
    Notes: Mit Pulspolarographie, Infrarot- und NMR-Spektroskopie sowie Elektronenanlagerungs-Massenspektrographie wurde die Hydrolyse von N-(2-Cyanäthylen-)harnstoff (BA 1) unter noch relativ milden Bedingungen (pH 5,6 bis 9,0; T = 37°C und 22°C) nachgewiesen. Die Hydrolysegeschwindigkeit nimmt mit steigendem pH-Wert zu. Bei pH 5,6 erfolgt die Hydrolyse sehr langsam (Halbwertszeit etwa 6 Tage), wobei auch schon Kondensationsprodukte nachweisbar sind. Bei pH 9,0 ist bereits nach 2 Tagen BA 1 unter Ringspaltung weitgehend hydrolysiert, und eine Reihe Kondensationsprodukte sind entstanden. Im mittleren pH-Bereich von 7,3 bis 8,3 wurde das Auftreten von 2-Cyanaziridin, aber auch schon Ringspaltung und hydrolytische Folgeprodukte beobachtet. Die Halbwertszeit der BA 1-Hydrolyse konnte bei pH 7,3, 37°C für eine 0,144 molare Lösung in Phosphatpuffer zu 103 ± 1 h bestimmt werden.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Journal für Praktische Chemie/Chemiker-Zeitung 319 (1977), S. 522-525 
    ISSN: 0021-8383
    Keywords: Chemistry ; Organic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: Polarographic Differentiation between 6-Azalumazines and 1,2,4-Triazines
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Journal für Praktische Chemie/Chemiker-Zeitung 320 (1978), S. 270-278 
    ISSN: 0021-8383
    Keywords: Chemistry ; Organic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: Polarographic Reduction of β-Aminovinylimines of the Indene SeriesThe mechanism of electrolytic reduction of aminovinylimine (AVI) is suggested, based on results of the identification of electrolysis products and on the dependence of polarographic curves. It is shown that this mechanism becomes complicated by the kinetics of hydrolysis of starting substances and intermediates. The determination of complex forming constants for AVI and bovine serum albumine is determined and compared by polarography and spectroscopy.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
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