Metabolic Tracing of NAD Precursors Using Strategically Labelled Isotopes of NMN
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Recipients of Honoris Causa Degrees and of Scholarships and Awards 1999
Recipients of Honoris Causa Degrees and of Scholarships and Awards 1999 Contents HONORIS CAUSA DEGREES OF THE UNIVERSITY OF MELBOURNE- Members of the Royal Family 1 Other Distinguished Graduates 1-9 SCHOLARSHIPS AND AWARDS- The Royal Commission of the Exhibition of 1851 Science Research Scholarships 1891-1988 10 Rhodes Scholars elected for Victoria 1904- 11 Royal Society's Rutherford Scholarship Holders 1952- 11 Aitchison Travelling Scholarship (from 1950 Aitchison-Myer) Holders 1927- 12 Sir Arthur Sims Travelling Scholarship Holders 1951- 12 Rae and Edith Bennett Travelling Scholarship Holders 1979- 13 Stella Mary Langford Scholarship Holders 1979- 13 University of Melbourne Travelling Scholarships Holders 1941-1983 14 Sir William Upjohn Medal 15 University of Melbourne Silver Medals 1966-1985 15 University of Melbourne Medals (new series) 1987 - Silver 16 Gold 16 31/12/99 RECIPIENTS OF HONORIS CAUSA DEGREES AND OF SCHOLARSHIPS AND AWARDS Honoris Causa Degrees of the University of Melbourne (Where recipients have degrees from other universities this is indicated in brackets after their names.) MEMBERS OF THE ROYAL FAMILY 1868 His Royal Highness Prince Alfred Ernest Albert, Duke of Edinburgh (Edinburgh) LLD 1901 His Royal Highness Prince George Frederick Ernest Albert, Duke of York (afterwards King George V) (Cambridge) LLD 1920 His Royal Highness Edward Albert Christian George Andrew Patrick David, Prince of Wales (afterwards King Edward VIII) (Oxford) LLD 1927 His Royal Highness Prince Albert Frederick Arthur George, -
DNA Repair Systems Guardians of the Genome
GENERAL ARTICLE DNA Repair Systems Guardians of the Genome D N Rao and Yedu Prasad The 2015 Nobel Prize in Chemistry was awarded jointly to Tomas Lindahl, Paul Modrich and Aziz Sancar to honour their accomplishments in the field of DNA repair. Ever since the discovery of DNA structure and their importance in the storage of genetic information, questions about their stability became pertinent. A molecule which is crucial for the de- velopment and propagation of an organism must be closely D N Rao is a professor at the monitored so that the genetic information is not corrupted. Department of Biochemistry, Thanks to the pioneering research work of Lindahl, Sancar, Indian Institute of Science, Modrich and their colleagues, we now have an holistic aware- Bengaluru. His research ness of how DNA damage occurs and how the damage is rec- work primarily focuses on DNA interacting proteins in tified in bacteria as well as in higher organisms including hu- prokaryotes. This includes man beings. A comprehensive understanding of DNA repair restriction-modification has proven crucial in the fight against cancer and other debil- systems, DNA repair proteins itating diseases. from pathogenic bacteria and and proteins involved in The genetic information that guides the development, metabolism horizontal gene transfer and and reproduction of all living organisms and many viruses resides DNA recombination. in the DNA. This biological information is stored in the DNA Yedu Prasad is a graduate molecule as combinations of sequences that are formed by purine student working on his PhD and pyrimidine bases attached to the deoxyribose sugar (Figure under the guidance of D N 1). -
Snps Related to Vitamin D and Breast Cancer Risk
Huss et al. Breast Cancer Research (2018) 20:1 DOI 10.1186/s13058-017-0925-3 RESEARCHARTICLE Open Access SNPs related to vitamin D and breast cancer risk: a case-control study Linnea Huss1* , Salma Tunå Butt1, Peter Almgren 2, Signe Borgquist3,4, Jasmine Brandt1, Asta Försti5,6, Olle Melander2 and Jonas Manjer1 Abstract Background: It has been suggested that vitamin D might protect from breast cancer, although studies on levels of vitamin D in association with breast cancer have been inconsistent. Genome-wide association studies (GWASs) have identified several single-nucleotide polymorphisms (SNPs) to be associated with vitamin D. The aim of this study was to investigate such vitamin D-SNP associations in relation to subsequent breast cancer risk. A first step included verification of these SNPs as determinants of vitamin D levels. Methods: The Malmö Diet and Cancer Study included 17,035 women in a prospective cohort. Genotyping was performed and was successful in 4058 nonrelated women from this cohort in which 865 were diagnosed with breast cancer. Levels of vitamin D (25-hydroxyvitamin D) were available for 700 of the breast cancer cases and 643 of unaffected control subjects. SNPs previously associated with vitamin D in GWASs were identified. Logistic regression analyses yielding ORs with 95% CIs were performed to investigate selected SNPs in relation to low levels of vitamin D (below median) as well as to the risk of breast cancer. Results: The majority of SNPs previously associated with levels of vitamin D showed a statistically significant association with circulating vitamin D levels. Heterozygotes of one SNP (rs12239582) were found to have a statistically significant association with a low risk of breast cancer (OR 0.82, 95% CI 0.68–0.99), and minor homozygotes of the same SNP were found to have a tendency towards a low risk of being in the group with low vitamin D levels (OR 0.72, 95% CI 0.52–1.00). -
N E W S I N B R I
N E W S I N B R I E F NOBEL PRIZE IN MEDICINE The Nobel Prize in Chemistry 2015 was awarded jointly to Tomas Lindahl, Paul Modrich and Aziz Sancar for elucidating At the height of the Vietnamese war, the common enemy of three different mechanisms by which errors occur in our DNA soldiers on either side of the battle lines was chloroquine- and the various mechanisms of DNA repair. In the 1970’s, resistant malaria. In 1964, the North Vietnamese Government Lindahl discovered that DNA undergoes regular decay and approached the Chinese leader Mao Tse Tung to find a damage. For example, cytosine loses an amino group to become solution to this deadly scourge. Mao immediately established uracil resulting in a mutation. Subsequently, he discovered an a military mission Project 523 with a main aim to discover a enzyme system called uracil-DNA glycosylase which corrects drug for resistant malaria. Youyou Tu was a phytochemist who this error. This process was called base excision repair. Aziz was in charge of the project. She and her team combed through Sancar discovered and cloned the gene for an enzyme called hundreds of old Chinese traditional medicine texts. Around photolyase which is critical in correcting DNA mutations caused 2000 chemicals extracted from various plants were evaluated. by high doses of UV exposure. He further went on to identify the Finally, they zeroed on to an extract of Artemesia annua L. exact chemical processes involved in this nucleotide excision also called Quinhao which was found to have excellent repair. Paul Modrich discovered the mechanism by which DNA antimalarial efficacy in a mouse model. -
9-Deoxy-A9,A12-13,14
Proc. Natl. Acad. Sci. USA Vol. 81, pp. 1317-1321, March 1984 Biochemistry 9-Deoxy-A9,A12-13,14-dihydroprostaglandin D2, a metabolite of prostaglandin D2 formed in human plasma (dehydration product of prostaglandin D2/serum albumin/cell growth inhibition) YOSHIHARU KIKAWA*, SHUH NARUMIYA*, MASANORI FUKUSHIMAt, HIROHISA WAKATSUKAt, AND OSAMU HAYAISHI§ *Department of Medical Chemistry, Kyoto University Faculty of Medicine, Sakyo-ku, Kyoto 606, Japan; tDepartment of Internal Medicine and Laboratory of Chemotherapy, Aichi Cancer Center, Chikusa-ku, Nagoya 464, Japan; tResearch Institute, Ono Pharmaceutical Co., Shimamoto, Mishima, Osaka 618, Japan; and §Osaka Medical College, Daigaku-cho, Takatsuki, Osaka 569, Japan Contributed by Osamu Hayaishi, November 8, 1983 ABSTRACT Incubation of prostaglandin D2 (PGD2) with from Sigma. Dimethylisopropylsilyl (Me2iPrSi) imidazole human plasma yielded a product that has been identified as 9- and methoxyamine hydrochloride were from Tokyo Kasei deoxy-9,10-didehydro-12,13-cdidehydro-13,14-dihydro-PGD2 (Tokyo). Sep-pak silica and Sep-pak C18 cartridges were (9-deoxy-_9,9'2-13,14-dihydro-PGD2). The identification was from Waters Associates. Precoated silica gel plates [G60- based on mass spectrometry, UV spectrometry, mobilities and (F254)] with concentration zones and silica gel 60 for column retention time on TLC and HPLC, and NMR. The conversion chromatography were from Merck. Sephadex LH-20 was a of PGD2 to this product was dependent on the incubation time product of Pharmacia. Solvents used in the extraction of and the amount of plasma added to a reaction mixture and was PGD2 metabolites for identification were distilled before use. abolished by prior boiling. -
Nicotinamide Riboside Kinases Display Redundancy in Mediating Nicotinamide Mononucleotide and Nicotinamide Riboside Metabolism in Skeletal Muscle Cells
Original Article Nicotinamide riboside kinases display redundancy in mediating nicotinamide mononucleotide and nicotinamide riboside metabolism in skeletal muscle cells Rachel S. Fletcher 1,2, Joanna Ratajczak 3,4, Craig L. Doig 1,2, Lucy A. Oakey 2, Rebecca Callingham 5, Gabriella Da Silva Xavier 5, Antje Garten 1,6, Yasir S. Elhassan 1,2, Philip Redpath 7, Marie E. Migaud 7, Andrew Philp 8, Charles Brenner 9, Carles Canto 3,4, Gareth G. Lavery 1,2,* ABSTRACT þ Objective: Augmenting nicotinamide adenine dinucleotide (NAD ) availability may protect skeletal muscle from age-related metabolic decline. þ Dietary supplementation of NAD precursors nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) appear efficacious in elevating þ þ muscle NAD . Here we sought to identify the pathways skeletal muscle cells utilize to synthesize NAD from NMN and NR and provide insight into mechanisms of muscle metabolic homeostasis. þ Methods: We exploited expression profiling of muscle NAD biosynthetic pathways, single and double nicotinamide riboside kinase 1/2 (NRK1/ þ 2) loss-of-function mice, and pharmacological inhibition of muscle NAD recycling to evaluate NMN and NR utilization. Results: Skeletal muscle cells primarily rely on nicotinamide phosphoribosyltransferase (NAMPT), NRK1, and NRK2 for salvage biosynthesis of þ þ NAD . NAMPT inhibition depletes muscle NAD availability and can be rescued by NR and NMN as the preferred precursors for elevating muscle þ cell NAD in a pathway that depends on NRK1 and NRK2. Nrk2 knockout mice develop normally and show subtle alterations to their NADþ metabolome and expression of related genes. NRK1, NRK2, and double KO myotubes revealed redundancy in the NRK dependent þ metabolism of NR to NAD . -
The Autobiography of Patience Loader Rozsa Archer
Utah State University DigitalCommons@USU All USU Press Publications USU Press 2006 Recollections of Past Days: The Autobiography of Patience Loader Rozsa Archer Sandra Ailey Petree Follow this and additional works at: https://digitalcommons.usu.edu/usupress_pubs Part of the United States History Commons Recommended Citation Archer, P. L., & Petree, S. A. (2006). Recollections of past days: The autobiography of Patience Loader Rozsa Archer. Logan, Utah: Utah State University Press. This Book is brought to you for free and open access by the USU Press at DigitalCommons@USU. It has been accepted for inclusion in All USU Press Publications by an authorized administrator of DigitalCommons@USU. For more information, please contact [email protected]. Recollections of Past Days The Autobiography of PATIENCE LOADER ROZSA ARCHER Edited by Sandra Ailey Petree Recollections of Past Days The Autobiography of Patience Loader Rozsa Archer Volume 8 Life Writings of Frontier Women A Series Edited by Maureen Ursenbach Beecher Volume 1 Winter Quarters The 1846 –1848 Life Writings of Mary Haskin Parker Richards Edited by Maurine Carr Ward Volume 2 Mormon Midwife The 1846 –1888 Diaries of Patty Bartlett Sessions Edited by Donna Toland Smart Volume 3 The History of Louisa Barnes Pratt Being the Autobiography of a Mormon Missionary Widow and Pioneer Edited by S. George Ellsworth Volume 4 Out of the Black Patch The Autobiography of Effi e Marquess Carmack Folk Musician, Artist, and Writer Edited by Noel A. Carmack and Karen Lynn Davidson Volume 5 The Personal Writings of Eliza Roxcy Snow Edited by Maureen Ursenbach Beecher Volume 6 A Widow’s Tale The 1884–1896 Diary of Helen Mar Kimball Whitney Transcribed and Edited by Charles M. -
Aziz SANCAR WINS Nobel Prize
Advancing SCIENCE Aziz Sancar, 2015 Nobel laureate in chemistry extremely proud that he is a member of TWAS, and we offer him heartfelt congratulations.” Sharing the prize with Sancar are two other chemists who have made pioneering discoveries in gene repair: Swedish native Tomas Lindahl of the Francis Crick Institute and Clare Hall Laboratory in Hertfordshire, UK, and American Paul Modrich of the Howard Hughes Medical Institute and Duke University School of Medicine in North Carolina. “Systematic work” by the three researchers “has made a decisive contribution to the understanding of how the living cell functions, as well as providing knowledge about the AZIZ SANCAR molecular causes of several hereditary diseases and about mechanisms behind both cancer development and WINS NOBEL PRIZE aging,” the Royal Swedish Academy of Sciences said in announcing the prizes. by Edward W. Lempinen Sancar, 69, was born in Savur, a small town in southeastern Turkey. The Turkish-born DNA to remove the damaged genetic He was the seventh of eight children. code. His initial discoveries at Yale “My parents were both illiterate,” he scientist, elected to TWAS University in the United States focused said in a 2005 profile published in the in 1994, shares the 2015 on E. coli bacteria; more recently, at Proceedings of the National Academy the University of North Carolina in the of Sciences (USA), “but they valued the Nobel Prize in chemistry United States, he detailed the workings importance of education and did their of this DNA repair in humans. best to ensure that all of their children for research into DNA Sancar is the first native of Turkey to would receive some education.” repair. -
(P -Value<0.05, Fold Change≥1.4), 4 Vs. 0 Gy Irradiation
Table S1: Significant differentially expressed genes (P -Value<0.05, Fold Change≥1.4), 4 vs. 0 Gy irradiation Genbank Fold Change P -Value Gene Symbol Description Accession Q9F8M7_CARHY (Q9F8M7) DTDP-glucose 4,6-dehydratase (Fragment), partial (9%) 6.70 0.017399678 THC2699065 [THC2719287] 5.53 0.003379195 BC013657 BC013657 Homo sapiens cDNA clone IMAGE:4152983, partial cds. [BC013657] 5.10 0.024641735 THC2750781 Ciliary dynein heavy chain 5 (Axonemal beta dynein heavy chain 5) (HL1). 4.07 0.04353262 DNAH5 [Source:Uniprot/SWISSPROT;Acc:Q8TE73] [ENST00000382416] 3.81 0.002855909 NM_145263 SPATA18 Homo sapiens spermatogenesis associated 18 homolog (rat) (SPATA18), mRNA [NM_145263] AA418814 zw01a02.s1 Soares_NhHMPu_S1 Homo sapiens cDNA clone IMAGE:767978 3', 3.69 0.03203913 AA418814 AA418814 mRNA sequence [AA418814] AL356953 leucine-rich repeat-containing G protein-coupled receptor 6 {Homo sapiens} (exp=0; 3.63 0.0277936 THC2705989 wgp=1; cg=0), partial (4%) [THC2752981] AA484677 ne64a07.s1 NCI_CGAP_Alv1 Homo sapiens cDNA clone IMAGE:909012, mRNA 3.63 0.027098073 AA484677 AA484677 sequence [AA484677] oe06h09.s1 NCI_CGAP_Ov2 Homo sapiens cDNA clone IMAGE:1385153, mRNA sequence 3.48 0.04468495 AA837799 AA837799 [AA837799] Homo sapiens hypothetical protein LOC340109, mRNA (cDNA clone IMAGE:5578073), partial 3.27 0.031178378 BC039509 LOC643401 cds. [BC039509] Homo sapiens Fas (TNF receptor superfamily, member 6) (FAS), transcript variant 1, mRNA 3.24 0.022156298 NM_000043 FAS [NM_000043] 3.20 0.021043295 A_32_P125056 BF803942 CM2-CI0135-021100-477-g08 CI0135 Homo sapiens cDNA, mRNA sequence 3.04 0.043389246 BF803942 BF803942 [BF803942] 3.03 0.002430239 NM_015920 RPS27L Homo sapiens ribosomal protein S27-like (RPS27L), mRNA [NM_015920] Homo sapiens tumor necrosis factor receptor superfamily, member 10c, decoy without an 2.98 0.021202829 NM_003841 TNFRSF10C intracellular domain (TNFRSF10C), mRNA [NM_003841] 2.97 0.03243901 AB002384 C6orf32 Homo sapiens mRNA for KIAA0386 gene, partial cds. -
Adrenaline Stimulates Glucagon Secretion by Tpc2-Dependent
1128 Diabetes Volume 67, June 2018 Adrenaline Stimulates Glucagon Secretion by Tpc2- Dependent Ca2+ Mobilization From Acidic Stores in Pancreatic a-Cells Alexander Hamilton,1 Quan Zhang,1 Albert Salehi,2 Mara Willems,1 Jakob G. Knudsen,1 Anna K. Ringgaard,3,4 Caroline E. Chapman,1 Alejandro Gonzalez-Alvarez,1 Nicoletta C. Surdo,5 Manuela Zaccolo,5 Davide Basco,6 Paul R.V. Johnson,1,7 Reshma Ramracheya,1 Guy A. Rutter,8 Antony Galione,9 Patrik Rorsman,1,2,7 and Andrei I. Tarasov1,7 Diabetes 2018;67:1128–1139 | https://doi.org/10.2337/db17-1102 Adrenaline is a powerful stimulus of glucagon secretion. It The ability of the “fight-or-flight” hormone adrenaline to acts by activation of b-adrenergic receptors, but the down- increase plasma glucose levels by stimulating liver gluconeo- stream mechanisms have only been partially elucidated. genesis is in part mediated by glucagon, the body’sprincipal Here, we have examined the effects of adrenaline in mouse hyperglycemic hormone (1). Glucagon is secreted by the and human a-cells by a combination of electrophysiology, a-cells of the pancreas (2). Reduced autonomic stimulation 2+ imaging of Ca and PKA activity, and hormone release of glucagon secretion may result in hypoglycemia, a serious measurements. We found that stimulation of glucagon and potentially fatal complication of diabetes (3). It has been secretion correlated with a PKA- and EPAC2-dependent estimated that up to 10% of insulin-treated patients die of (inhibited by PKI and ESI-05, respectively) elevation of hypoglycemia (4). Understanding the mechanism by which [Ca2+] in a-cells, which occurred without stimulation of i adrenaline stimulates glucagon secretion and how it becomes ISLET STUDIES electrical activity and persisted in the absence of extracel- perturbed in patients with diabetes is therefore essential. -
Synthesis of the Ca -Mobilizing Messengers NAADP
ARTICLE cro Author’s Choice Synthesis of the Ca2؉-mobilizing messengers NAADP and cADPR by intracellular CD38 enzyme in the mouse heart: Role in -adrenoceptor signaling Received for publication, April 3, 2017, and in revised form, May 13, 2017 Published, Papers in Press, May 24, 2017, DOI 10.1074/jbc.M117.789347 Wee K. Lin‡, Emma L. Bolton‡, Wilian A. Cortopassi§¶, Yanwen Wangʈ, Fiona O’Brien‡, Matylda Maciejewska‡, Matthew P. Jacobson¶, Clive Garnham‡, Margarida Ruas‡, John Parrington‡, Ming Lei‡1, Rebecca Sitsapesan‡2, Antony Galione‡3, and Derek A. Terrar‡4 From the ‡Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, United Kingdom, the §Department of Chemistry, Chemistry Research Laboratory, University of Oxford, Mansfield Road, Oxford OX1 3TA, United Kingdom, the ¶Department of Pharmaceutical Chemistry, University of California, San Francisco, California 94158, and the ʈFaculty of Biology, Medicine, and Health, University of Manchester, Manchester M13 9NT, United Kingdom Edited by Roger J. Colbran Nicotinic acid adenine dinucleotide phosphate (NAADP) and increase both Ca2؉ transients and the tendency to disturb .cyclic ADP-ribose (cADPR) are Ca2؉-mobilizing messengers heart rhythm important for modulating cardiac excitation–contraction cou- pling and pathophysiology. CD38, which belongs to the ADP- ribosyl cyclase family, catalyzes synthesis of both NAADP and ADP-ribosyl cyclases (ARCs)5 are enzymes capable of con- cADPR in vitro. However, it remains unclear whether this is the verting NAD into cyclic adenosine diphosphate ribose main enzyme for their production under physiological condi- (cADPR). In addition, some of these cyclases (for example, tions. Here we show that membrane fractions from WT but not CD38 and Aplysia cyclase), can (at least under in vitro condi- ؊/؊ CD38 mouse hearts supported NAADP and cADPR synthe- tions) also produce nicotinic acid adenine dinucleotide phos- sis. -
Open Data for Differential Network Analysis in Glioma
International Journal of Molecular Sciences Article Open Data for Differential Network Analysis in Glioma , Claire Jean-Quartier * y , Fleur Jeanquartier y and Andreas Holzinger Holzinger Group HCI-KDD, Institute for Medical Informatics, Statistics and Documentation, Medical University Graz, Auenbruggerplatz 2/V, 8036 Graz, Austria; [email protected] (F.J.); [email protected] (A.H.) * Correspondence: [email protected] These authors contributed equally to this work. y Received: 27 October 2019; Accepted: 3 January 2020; Published: 15 January 2020 Abstract: The complexity of cancer diseases demands bioinformatic techniques and translational research based on big data and personalized medicine. Open data enables researchers to accelerate cancer studies, save resources and foster collaboration. Several tools and programming approaches are available for analyzing data, including annotation, clustering, comparison and extrapolation, merging, enrichment, functional association and statistics. We exploit openly available data via cancer gene expression analysis, we apply refinement as well as enrichment analysis via gene ontology and conclude with graph-based visualization of involved protein interaction networks as a basis for signaling. The different databases allowed for the construction of huge networks or specified ones consisting of high-confidence interactions only. Several genes associated to glioma were isolated via a network analysis from top hub nodes as well as from an outlier analysis. The latter approach highlights a mitogen-activated protein kinase next to a member of histondeacetylases and a protein phosphatase as genes uncommonly associated with glioma. Cluster analysis from top hub nodes lists several identified glioma-associated gene products to function within protein complexes, including epidermal growth factors as well as cell cycle proteins or RAS proto-oncogenes.