Purines and Pyrimidines Panel, Urine

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FILE DEFINITION TEST CHANGE Notification Date: October 11, 2019 Effective Date: November 14, 2019 Purines and Pyrimidines Panel, Urine Test ID: PUPYU Explanation: On 11/14/19, a new reportable field for S-Sulfocysteine will be added to the test. The reference ranges for the test will also be updated to include the analyte. Collaborative Laboratory Integrated Reports (CLIR) images will be available for viewing via a Supplemental Report in Mayo Access. These images will be added to the report at the discretion of the signing consultant. Accessing Supplemental PDF Reports in Mayo Access - questions on this process can be directed to MCL Client Support. Current Result Codes New Result Codes Result ID Reporting Name Result ID Reporting Name 42201 Interpretation (PUPYU) 42201 Interpretation (PUPYU) 41978 Uracil 41978 Uracil 38249 Thymine 38249 Thymine 38239 Adenine 38239 Adenine 41980 Hypoxanthine 41980 Hypoxanthine 41981 Xanthine 41981 Xanthine 38246 Orotic Acid 38246 Orotic Acid 38251 Dihydroorotic 38251 Dihydroorotic 41979 Uric Acid 41979 Uric Acid 38252 Deoxythymidine 38252 Deoxythymidine 38253 Deoxyuridine 38253 Deoxyuridine 38248 Thymidine 38248 Thymidine 38250 Uridine 38250 Uridine 38241 Deoxyadenosine 38241 Deoxyadenosine 38243 Deoxyinosine 38243 Deoxyinosine © Mayo Foundation for Medical Education and Research. All rights reserved. 1 of 2 38242 Deoxyguanosine 38242 Deoxyguanosine 38240 Adenosine 38240 Adenosine 38245 Inosine 38245 Inosine 38244 Guanosine 38244 Guanosine 38254 AICAR 38254 AICAR 38247 Succinyladenosine 38247 Succinyladenosine 38255 Dihydrouracil 606745 S-Sulfocysteine 38256 Dihydrothymine 38255 Dihydrouracil 38257 N-carbamoyl-beta-alanine 38256 Dihydrothymine 38258 N-carbamoyl-beta-aminoisobutyric Acid 38257 N-carbamoyl-beta-alanine 42200 Reviewed By 38258 N-carbamoyl-beta-aminoisobutyric Acid 42200 Reviewed By Current Reference Value* N/A New Reference Value 0-3 Years 4-6 Years 7-12 Years 13-18 Years >18 Years mmol/mol mmol/mol mmol/mol mmol/mol mmol/mol creatinine creatinine creatinine creatinine creatinine S-Sulfocysteine < or =11 < or =5 < or =5 < or =5 < or =5 *Reference values for all other analytes tested in the assay are not changing. See the PUPYU Lab Test Catalog for details. Questions Contact Melissa Tricker-Klar, Laboratory Technologist Resource Coordinator at 800-533-1710. © Mayo Foundation for Medical Education and Research. All rights reserved. 2 of 2 .

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Thesis Final
CHARACTERIZATION OF ADENOSINE NUCLEOSIDASE FROM ALASKA PEA SEEDS by Abdullah K. Shamsuddin A Thesis Submitted to the Faculty of the College of Graduate Studies at Middle Tennessee State University in Partial Fulfillment of the Requirements for the Degree of Master of Science in Chemistry Middle Tennessee State University August 2015 Thesis Committee: Dr. Paul C. Kline, Chair Dr. Donald A. Burden Dr. Kevin L. Bicker I dedicate this research to my parents, my sisters, and my brother. I love you all. ii" " ACKNOWLEDGEMENTS I would like to express my sincere gratitude to my advisor, Dr. Paul C. Kline, for his guidance, support, and ongoing encouragement throughout this project. I also wish to thank my committee members, Dr. Donald A. Burden and Dr. Kevin L. Bicker, for their advice and insightful comments. In addition, I would like to thank all the staff and faculty of the Department of Chemistry for their contribution to the success of this study. Lastly, I wish to thank my family and my friends, without whom none of my accomplishments would have been possible. Thank you for you endless support, concern, love, and prayer. iii" " ABSTRACT Adenosine nucleosidase was purified from Alaska pea seeds five days after germination. A 4-fold purification has been reached with a 1.3 % recovery. The subunit molecular weight of adenosine nucleosidase was determined by mass spectrometry to be 26,103 daltons. The number of subunits was 1. The Michaelis constant, Km, and the maximum velocity, V max, for adenosine were determined to be 137 ± 48 µM, and 0.34 ± 0.02 µM/min respectively.
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Pyrimidine Base Degradation in Cultured Murine C-1300 Neuroblastoma Cells and in Situ Tumors
Pyrimidine base degradation in cultured murine C-1300 neuroblastoma cells and in situ tumors. M Tuchman, … , M L Ramnaraine, B L Mirkin J Clin Invest. 1988;81(2):425-430. https://doi.org/10.1172/JCI113336. Research Article Dihydropyrimidine dehydrogenase (DPD), the initial, rate-limiting step in pyrimidine degradation, was studied in two cell lines of murine neuroblastoma (MNB-T1 and MNB-T2) that were derived from C-1300 MNB tumor carried in A/J mice. The MNB-T2 (low malignancy) cell line was originally derived from the in situ tumor and carried in tissue culture for more than 100 passages; the MNB-T1 (high malignancy) line consisted of a new sub-culture that was also established from the in situ MNB tumor. DPD activity was determined in cytosolic preparations of MNB utilizing high performance liquid chromatography to separate the radiolabeled substrate ([2-14C]thymine) from [2-14C]dihydrothymine. The apparent affinity of DPD for NADPH in MNB cells (Km approximately 0.08 mM) was identical to that of A/J mouse brain and liver. The DPD activity of the high malignancy (MNB-T1) cell line was 14.3% of that observed in the low malignancy (MNB-T2) line. In situ tumors formed after implantation of high malignancy (MNB-T1) cells into A/J mice had only 25.2% of the DPD activity observed in tumors derived from low malignancy (MNB-T2) cells. When MNB-T2 cells were injected into naive A/J mice, tumors developed in only 68% of animals, the tumor growth rate was slow and a mortality of 20% was observed.
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(10) Patent No.: US 8119385 B2
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Induced Alterations in the Urine Metabolome in Cardiac Surgery
www.nature.com/scientificreports OPEN Bretschneider solution- induced alterations in the urine metabolome in cardiac surgery Received: 16 August 2018 Accepted: 1 November 2018 patients Published: xx xx xxxx Cheng-Chia Lee1,3, Ya-Ju Hsieh 2, Shao-Wei Chen3,4, Shu-Hsuan Fu2, Chia-Wei Hsu 2, Chih-Ching Wu 2,5,6, Wei Han7, Yunong Li7, Tao Huan7, Yu-Sun Chang2,6,8, Jau-Song Yu2,9,10, Liang Li7, Chih-Hsiang Chang1,3 & Yi-Ting Chen 1,2,11,12 The development of Bretschneider’s histidine-tryptophan-ketoglutarate (HTK) cardioplegia solution represented a major advancement in cardiac surgery, ofering signifcant myocardial protection. However, metabolic changes induced by this additive in the whole body have not been systematically investigated. Using an untargeted mass spectrometry-based method to deeply explore the urine metabolome, we sought to provide a holistic and systematic view of metabolic perturbations occurred in patients receiving HTK. Prospective urine samples were collected from 100 patients who had undergone cardiac surgery, and metabolomic changes were profled using a high-performance chemical isotope labeling liquid chromatography-mass spectrometry (LC-MS) method. A total of 14,642 peak pairs or metabolites were quantifed using diferential 13C-/12C-dansyl labeling LC-MS, which targets the amine/phenol submetabolome from urine specimens. We identifed 223 metabolites that showed signifcant concentration change (fold change > 5) and assembled several potential metabolic pathway maps derived from these dysregulated metabolites. Our data indicated upregulated histidine metabolism with subsequently increased glutamine/glutamate metabolism, altered purine and pyrimidine metabolism, and enhanced vitamin B6 metabolism in patients receiving HTK.
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Particular Metabolic Profile of Patient with Total
International Journal of Pharmaceutical Science and Health Care Issue 5, Vol. 1 (Jan-Feb. 2015) Available online on http://www.rspublication.com/ijphc/index.html ISSN 2249 – 5738 PARTICULAR METABOLIC PROFILE OF PATIENT WITH TOTAL DIHYDROPYRIMIDINE DEHYDROGENASE DEFICIENCY (DPD) Saif Eddine GAMAOUNa,b, Nissem ABDEJALLILa, Mhamed Ali HAMZAb, Saad SAGUEMa aLaboratory of Metabolic Biophysics, Professional and Applied Environmental Toxicology, Medicine faculty of Sousse, Mohamed Karoui street, Sousse 4002, Tunisia bDepartment of chemistry, sciences faculty of Monastir, Environment street, Monastir 5019, Tunisia *Author for correspondence at present address: Saif Eddine GAMAOUN Higher Institute of Technological Studies (ISET) Ksar Hellal-Hadj Ali Soua street-5070-Ksar Hellal,Tunisia Fonction : Engineer of analytical chemistry and instrumentation - Assistant teacher in ISET Ksar Hellal - Tunisia Tel.: (+216) 73 475 900 / (+216) 98 685 958 Fax: (+216) 73 475 163 E-mail: saifeddineg @ yahoo.fr ABSTRACT 5-Fluorouracil (5-FU) remains one of the most used chemotherapeutics agents in the treatment of several types of cancers. Its use could nevertheless, raise a problem of pharmacovigilance. It may engender a very grave toxicity which can be fatal at certain patient's presenting an enzymatic deficit with dihydropyrimidine dehydrogenase (DPD). The identification of the subjects at risk through the detection of a partial or total deficit before starting the treatment with 5-FU, could allow to adapt individually the prescribed dose, to optimize the therapeutic efficacy and reduce potential toxicities at expanding patients of a partial deficit to DPD. Such a screening would especially become more important when it is about a complete deficit in DPD. Such metabolic abnormality whose frequency is of the order of one per thousand, would indeed constitute a contraindication absolved from any chemotherapy with 5-FU (mortal toxicities).
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Vol. 2, 1937-1 941, December 1996 Clinical Cancer Research 1937 Possible Prediction of Adverse Reactions to Pyrimidine Chemotherapy from Urinary Pyrimidine Levels and a Case of Asymptomatic Adult Dihydropyrimidinuria1 Katsuo Hayashi,2 Kiyoshi Kidouchi, INTRODUCTION Satoshi Sumi, Masashi Mizokami, Etsuro Onto, Pyrimidine chemotherapy agents such as 5-FU3 are used widely but can occasionally cause serious adverse reactions. In Kazunoni Kumada, Ryuzo Ueda, and pyrimidine metabolism, uracil and thymine are first converted to Yoshino Wada dihydropyrimidines (dihydrouracil and dihydrothymine) by Departments of Medicine [K. H., K. Ku.] and Pediatrics [K. Ki.], DPD and then are metabolized to 3-ureidopropionic acid and Nagoya City Higashi General Hospital, 2-23 Wakamizu 1-chome, 3-ureidoisobutyric acid, respectively, by dihydropyrimidinase. Chikusa-ku, Nagoya 464, Japan, and Department of Pediatrics [S. S., These compounds are converted subsequently into 3-alanine Y. W.] and Second Department of Medicine [M. M., E. 0., R. U.], Nagoya City University Medical School. Nagoya, Japan and -arninoisobutyric acid, respectively ( 1). Because about 80% of an administered dose of 5-FU is degraded by this pathway, there is a possibility of adverse reactions occurring as ABSTRACT a result of DPD or dihydrophrimidinase deficiency. The value of Deficiency of dihydropyrimidine dehydrogenase or di- measuring peripheral blood monocyte DPD activity before ad- hydropyrimidinase, enzymes that catalyze the breakdown of ministering 5-FU has been suggested in Western countries (2- pyrimidine chemotherapy agents such as 5-fluorouracil, 6), but DPD deficiency has not been reported in Japan. may cause serious adverse reactions to these agents. We Using a method that permits analysis of dihydrouracil and attempted to establish the reference range for urinary pyri- uracil in small volumes of urine, we previously screened Japa- midines in adults to detect individuals with abnormal py- nese infants for abnormalities of pyrimidine metabolism and rimidine metabolism.
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Ung)-Initiated Dna Base Excision Repair in The
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