DOCSLIB.ORG

EC by Tree 2021

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
EC by Tree 2021 Mn: A02 Term: Musculoskeletal System Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D006321 Heart chemistry Myocardium chemistry cytology Myocardium cytology enzymology Myocardium enzymology immunology Myocardium immunology metabolism Myocardium metabolism pathology Myocardium pathology ultrastructure Myocardium ultrastructure Mn: A03 Term: Digestive System Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D007422 Intestines metabolism Intestinal Mucosa metabolism D013270 Stomach metabolism Gastric Mucosa metabolism Mn: A04 Term: Respiratory System Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D009666 Nose metabolism Nasal Mucosa metabolism Mn: A07 Term: Cardiovascular System Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D006321 Heart blood supply Coronary Vessels chemistry Myocardium chemistry cytology Myocardium cytology enzymology Myocardium enzymology immunology Myocardium immunology metabolism Myocardium metabolism pathology Myocardium pathology ultrastructure Myocardium ultrastructure D009206 Myocardium anatomy & histology Heart anatomy & histology blood supply Coronary Vessels diagnostic imaging Heart diagnostic imaging drug effects Heart drug effects embryology Heart embryology growth & development Heart growth & development Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D009206 Myocardium innervation Heart innervation microbiology Heart microbiology parasitology Heart parasitology physiology Heart physiology physiopathology Heart physiopathology radiation effects Heart radiation effects virology Heart virology Mn: A08 Term: Nervous System Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D007830 Larynx innervation Laryngeal Nerves Mn: A10 Term: Tissues Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D006321 Heart chemistry Myocardium chemistry cytology Myocardium cytology enzymology Myocardium enzymology immunology Myocardium immunology metabolism Myocardium metabolism pathology Myocardium pathology ultrastructure Myocardium ultrastructure D007422 Intestines metabolism Intestinal Mucosa metabolism D009666 Nose metabolism Nasal Mucosa metabolism D013270 Stomach metabolism Gastric Mucosa metabolism Mn: A11 Term: Cells Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D001769 Blood cytology Blood Cells D001853 Bone Marrow cytology Bone Marrow Cells D003238 Connective Tissue cytology Connective Tissue Cells D004817 Epidermis cytology Epidermal Cells D004848 Epithelium cytology Epithelial Cells D004912 Erythrocytes abnormalities Erythrocytes, Abnormal D010944 Plants cytology Plant Cells Mn: A12 Term: Fluids and Secretions Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D014867 Water blood Blood urine Urine Mn: A13 Term: Animal Structures Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D002645 Chickens embryology Chick Embryo Mn: A15 Term: Hemic and Immune Systems Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D001769 Blood cytology Blood Cells D001853 Bone Marrow cytology Bone Marrow Cells D004912 Erythrocytes abnormalities Erythrocytes, Abnormal D014867 Water blood Blood Mn: A16 Term: Embryonic Structures Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D002645 Chickens embryology Chick Embryo Mn: C01 Term: Infections Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D006373 Helminthiasis veterinary Helminthiasis, Animal D006505 Hepatitis veterinary Hepatitis, Animal D010272 Parasitic Diseases veterinary Parasitic Diseases, Animal D011528 Protozoan Infections veterinary Protozoan Infections, Animal D012480 Salmonella Infections veterinary Salmonella Infections, Animal D013587 Syphilis congenital Syphilis, Congenital D014123 Toxoplasmosis congenital Toxoplasmosis, Congenital veterinary Toxoplasmosis, Animal D014125 Toxoplasmosis, Congenital veterinary Toxoplasmosis, Animal congenital Mn: C04 Term: Neoplasms Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D009369 Neoplasms secondary Neoplasm Metastasis D051760 Xeroderma Pigmentosum Group A deficiency Xeroderma Protein Pigmentosum Mn: C05 Term: Musculoskeletal Diseases Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D005121 Extremities abnormalities Limb Deformities, Congenital D005528 Foot abnormalities Foot Deformities, Congenital D005530 Foot Deformities congenital Foot Deformities, Congenital D006132 Growth Plate injuries Salter-Harris Fractures D006225 Hand abnormalities Hand Deformities, Congenital D006226 Hand Deformities congenital Hand Deformities, Congenital D006617 Hip Dislocation congenital Hip Dislocation, Congenital D007037 Hypothyroidism congenital Congenital Hypothyroidism D007568 Jaw abnormalities Jaw Abnormalities D035002 Lower Extremity abnormalities Lower Extremity Deformities, Congenital D009141 Musculoskeletal System abnormalities Musculoskeletal Abnormalities D009211 Myoglobin urine Myoglobinuria D009222 Myotonia congenital Myotonia Congenita D009230 Myxedema congenital Congenital Hypothyroidism D053402 PHEX Phosphate Regulating Neutral deficiency Familial Hypophosphatemic Endopeptidase Rickets D025203 Phosphofructokinase-1, Muscle Type deficiency Glycogen Storage Disease Type VII D055758 SOX9 Transcription Factor deficiency Campomelic Dysplasia D053773 Transforming Growth Factor beta1 deficiency Camurati-Engelmann Syndrome D034941 Upper Extremity abnormalities Upper Extremity Deformities, Congenital Mn: C06 Term: Digestive System Diseases Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D003304 Coproporphyrinogen deficiency Coproporphyria, Hereditary Oxidase D004064 Digestive System abnormalities Digestive System Abnormalities Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D005294 Ferrochelatase deficiency Protoporphyria, Erythropoietic D006505 Hepatitis veterinary Hepatitis, Animal D006521 Hepatitis, Chronic chemically Chemical and Drug Induced Liver induced Injury, Chronic D011163 Hydroxymethylbilane deficiency Porphyria, Acute Intermittent Synthase D008107 Liver Diseases chemically Chemical and Drug Induced Liver Injury induced D008531 Megacolon congenital Hirschsprung Disease D050768 Protoporphyrinogen deficiency Porphyria, Variegate Oxidase D000515 alpha 1-Antitrypsin deficiency alpha 1-Antitrypsin Deficiency Mn: C07 Term: Stomatognathic Diseases Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D005154 Facial Nerve injuries Facial Nerve Injuries D007568 Jaw abnormalities Jaw Abnormalities D008036 Lingual Nerve injuries Lingual Nerve Injuries D008340 Mandibular Nerve injuries Mandibular Nerve Injuries D009055 Mouth abnormalities Mouth Abnormalities D013284 Stomatognathic System abnormalities Stomatognathic System Abnormalities D014070 Tooth abnormalities Tooth Abnormalities injuries Tooth Injuries D014276 Trigeminal Nerve injuries Trigeminal Nerve Injuries Mn: C08 Term: Respiratory Tract Diseases Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D001608 Beryllium poisoning Berylliosis D007823 Laryngeal Nerves injuries Laryngeal Nerve Injuries D008168 Lung injuries Lung Injury D012009 Recurrent Laryngeal Nerve injuries Recurrent Laryngeal Nerve Injuries D012137 Respiratory System abnormalities Respiratory System Abnormalities D000515 alpha 1-Antitrypsin deficiency alpha 1-Antitrypsin Deficiency Mn: C09 Term: Otorhinolaryngologic Diseases Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D007823 Laryngeal Nerves injuries Laryngeal Nerve Injuries D012009 Recurrent Laryngeal Nerve injuries Recurrent Laryngeal Nerve Injuries D000159 Vestibulocochlear Nerve injuries Vestibulocochlear Nerve Injuries Mn: C10 Term: Nervous System Diseases Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D015632 1-Methyl-4-phenyl-1,2,3,6- poisoning MPTP Poisoning tetrahydropyridine toxicity MPTP Poisoning D000010 Abducens Nerve injuries Abducens Nerve Injury D000055 Accessory Nerve injuries Accessory Nerve Injuries D055573 Acid Ceramidase deficiency Farber Lipogranulomatosis D001119 Arginase deficiency Hyperargininemia D001123 Argininosuccinate Lyase deficiency Argininosuccinic Aciduria D001151 Arsenic poisoning Arsenic Poisoning D001152 Arsenicals poisoning Arsenic Poisoning toxicity Arsenic Poisoning D001921 Brain injuries Brain Injuries D002339 Carotid Arteries injuries Carotid Artery Injuries D017536 Carotid Artery, Common injuries Carotid Artery Injuries D002342 Carotid Artery, External injuries Carotid Artery Injuries D002343 Carotid Artery, Internal injuries Carotid Artery Injuries D053181 Caspase 8 deficiency Alstrom Syndrome D003315 Cornea injuries Corneal Injuries D003337 Corpus Callosum abnormalities Agenesis of Corpus Callosum D003391 Cranial Nerves injuries Cranial Nerve Injuries D004093 Dihydropteridine Reductase deficiency Phenylketonurias D020820 Dyskinesias chemically Dyskinesia, Drug-Induced induced D005123 Eye injuries Eye Injuries D005145 Face injuries Facial Injuries D005154 Facial Nerve injuries Facial Nerve Injuries D051860 Fragile X Mental Retardation deficiency Fragile X Syndrome Protein D005930 Glossopharyngeal Nerve injuries Glossopharyngeal Nerve Injuries D006257 Head injuries Craniocerebral Trauma D054819 Hexosaminidase B deficiency Sandhoff Disease Desc Ui Term Qualifier EC MeSH Heading New Qualifier if needed D007002 Hypoglossal Nerve injuries Hypoglossal Nerve Injuries D007066 Iduronate Sulfatase deficiency Mucopolysaccharidosis II D007823 Laryngeal Nerves injuries Laryngeal Nerve Injuries D008036 Lingual Nerve injuries Lingual Nerve
Load more

Recommended publications
  • 35 Disorders of Purine and Pyrimidine Metabolism
    35 Disorders of Purine and Pyrimidine Metabolism Georges van den Berghe, M.- Françoise Vincent, Sandrine Marie 35.1 Inborn Errors of Purine Metabolism – 435 35.1.1 Phosphoribosyl Pyrophosphate Synthetase Superactivity – 435 35.1.2 Adenylosuccinase Deficiency – 436 35.1.3 AICA-Ribosiduria – 437 35.1.4 Muscle AMP Deaminase Deficiency – 437 35.1.5 Adenosine Deaminase Deficiency – 438 35.1.6 Adenosine Deaminase Superactivity – 439 35.1.7 Purine Nucleoside Phosphorylase Deficiency – 440 35.1.8 Xanthine Oxidase Deficiency – 440 35.1.9 Hypoxanthine-Guanine Phosphoribosyltransferase Deficiency – 441 35.1.10 Adenine Phosphoribosyltransferase Deficiency – 442 35.1.11 Deoxyguanosine Kinase Deficiency – 442 35.2 Inborn Errors of Pyrimidine Metabolism – 445 35.2.1 UMP Synthase Deficiency (Hereditary Orotic Aciduria) – 445 35.2.2 Dihydropyrimidine Dehydrogenase Deficiency – 445 35.2.3 Dihydropyrimidinase Deficiency – 446 35.2.4 Ureidopropionase Deficiency – 446 35.2.5 Pyrimidine 5’-Nucleotidase Deficiency – 446 35.2.6 Cytosolic 5’-Nucleotidase Superactivity – 447 35.2.7 Thymidine Phosphorylase Deficiency – 447 35.2.8 Thymidine Kinase Deficiency – 447 References – 447 434 Chapter 35 · Disorders of Purine and Pyrimidine Metabolism Purine Metabolism Purine nucleotides are essential cellular constituents 4 The catabolic pathway starts from GMP, IMP and which intervene in energy transfer, metabolic regula- AMP, and produces uric acid, a poorly soluble tion, and synthesis of DNA and RNA. Purine metabo- compound, which tends to crystallize once its lism can be divided into three pathways: plasma concentration surpasses 6.5–7 mg/dl (0.38– 4 The biosynthetic pathway, often termed de novo, 0.47 mmol/l). starts with the formation of phosphoribosyl pyro- 4 The salvage pathway utilizes the purine bases, gua- phosphate (PRPP) and leads to the synthesis of nine, hypoxanthine and adenine, which are pro- inosine monophosphate (IMP).
    [Show full text]
  • Purine Metabolism in Cultured Endothelial Cells
    PURINE METABOLISM IN MAN-III Biochemical, Immunological, and Cancer Research Edited by Aurelio Rapado Fundacion Jimenez Diaz Madrid, Spain R.W.E. Watts M.R.C. Clinical Research Centre Harrow, England and Chris H.M.M. De Bruyn Department of Human Genetics University of Nijmegen Faculty of Medicine Nijmegen, The Netherlands PLENUM PRESS · NEW YORK AND LONDON Contents of Part Β I. PURINE METABOLISM PATHWAYS AND REGULATION A. De Novo Synthesis; Precursors and Regulation De Novo Purine Synthesis in Cultured Human Fibroblasts 1 R.B. Gordon, L. Thompson, L.A. Johnson, and B.T. Emmerson Comparative Metabolism of a New Antileishmanial Agent, Allopurinol Riboside, in the Parasite and the Host Cell 7 D. J. Nelson, S.W. LaFon, G.B. Elion, J.J. Marr, and R.L. Berens Purine Metabolism in Rat Skeletal Muscle 13 E. R. Tully and T.G. Sheehan Alterations in Purine Metabolism in Cultured Fibroblasts with HGPRT Deficiency and with PRPPP Synthetase Superactivity 19 E. Zoref-Shani and 0. Sperling Purine Metabolism in Cultured Endothelial Cells 25 S. Nees, A.L. Gerbes, B. Willershausen-Zönnchen, and E. Gerlach Determinants of 5-Phosphoribosyl-l-Pyrophosphate (PRPP) Synthesis in Human Fibroblasts 31 K.0, Raivio, Ch. Lazar, H. Krumholz, and M.A. Becker Xanthine Oxidoreductase Inhibition by NADH as a Regulatory Factor of Purine Metabolism 35 M.M. Jezewska and Z.W. Kaminski vii viii CONTENTS OF PART Β Β. Nucleotide Metabolism Human Placental Adenosine Kinase: Purification and Characterization 41 CM. Andres, T.D. Palella, and I.H. Fox Long-Term Effects of Ribose on Adenine Nucleotide Metabolism in Isoproterenol-Stimulated Hearts .
    [Show full text]
  • 367.Full.Pdf
    Human Complement Factor I Does Not Require Cofactors for Cleavage of Synthetic Substrates This information is current as Stefanos A. Tsiftsoglou and Robert B. Sim of October 2, 2021. J Immunol 2004; 173:367-375; ; doi: 10.4049/jimmunol.173.1.367 http://www.jimmunol.org/content/173/1/367 Downloaded from References This article cites 41 articles, 17 of which you can access for free at: http://www.jimmunol.org/content/173/1/367.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on October 2, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2004 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Human Complement Factor I Does Not Require Cofactors for Cleavage of Synthetic Substrates1 Stefanos A. Tsiftsoglou2 and Robert B. Sim Complement factor I (fI) plays a major role in the regulation of the complement system. It circulates in an active form and has very restricted specificity, cleaving only C3b or C4b in the presence of a cofactor such as factor H (fH), complement receptor type 1, membrane cofactor protein, or C4-binding protein.
    [Show full text]
  • THE EFFECTS of ENVIRONMENTAL and PHYSICAL STRESS on ENERGY EXPENDITURE, ENERGY INTAKE, and APPETITE by Iva Mandic a Thesis Subm
    THE EFFECTS OF ENVIRONMENTAL AND PHYSICAL STRESS ON ENERGY EXPENDITURE, ENERGY INTAKE, AND APPETITE by Iva Mandic A thesis submitted in conformity with the requirements for the degree of Doctor of Philosophy Graduate Department of Exercise Science University of Toronto © Copyright by Iva Mandic (2018) The effects of environmental and physical stress on energy expenditure, energy intake, and appetite Iva Mandic Doctor of Philosophy The Graduate Department of Exercise Sciences University of Toronto 2018 Abstract Body weight loss occurs frequently in military personnel engaged in field operations. When this weight loss is rapid, or extensive it is associated with health and performance decrements. While the nature of military work does not allow for energy expenditure (EE) to be freely altered, energy intake (EI) can be increased to match EE and prevent weight loss. Therefore a primary objective of the current dissertation was to develop a physiological and empirical basis to facilitate informed estimates of the EI that would be required to offset the EE demand of military tasks during field operations. Three different approaches were undertaken: 1) The energy costs of 46 infantry tasks were measured; the results should reduce the dependency on less accurate predictions. 2) The impact of ambient temperature on EE of the tasks was minimal (~3%) when the ambient temperature was between -10°C and 30°C. This indicates that caloric supplementation of field rations on account of temperature is likely unnecessary during short-term operations occurring within this temperature range; and, lastly 3) A simple algorithm based on accelerometry and heart rate was developed to assess EE in the field.
    [Show full text]
  • Multiple Technology Appraisal Avatrombopag and Lusutrombopag
    Multiple Technology Appraisal Avatrombopag and lusutrombopag for treating thrombocytopenia in people with chronic liver disease needing an elective procedure [ID1520] Committee papers © National Institute for Health and Care Excellence 2019. All rights reserved. See Notice of Rights. The content in this publication is owned by multiple parties and may not be re-used without the permission of the relevant copyright owner. NATIONAL INSTITUTE FOR HEALTH AND CARE EXCELLENCE MULTIPLE TECHNOLOGY APPRAISAL Avatrombopag and lusutrombopag for treating thrombocytopenia in people with chronic liver disease needing an elective procedure [ID1520] Contents: 1 Pre-meeting briefing 2 Assessment Report prepared by Kleijnen Systematic Reviews 3 Consultee and commentator comments on the Assessment Report from: • Shionogi 4 Addendum to the Assessment Report from Kleijnen Systematic Reviews 5 Company submission(s) from: • Dova • Shionogi 6 Clarification questions from AG: • Questions to Shionogi • Clarification responses from Shionogi • Questions to Dova • Clarification responses from Dova 7 Professional group, patient group and NHS organisation submissions from: • British Association for the Study of the Liver (BASL) The Royal College of Physicians supported the BASL submission • British Society of Gastroenterology (BSG) 8 Expert personal statements from: • Vanessa Hebditch – patient expert, nominated by the British Liver Trust • Dr Vickie McDonald – clinical expert, nominated by British Society for Haematology • Dr Debbie Shawcross – clinical expert, nominated by Shionogi © National Institute for Health and Care Excellence 2019. All rights reserved. See Notice of Rights. The content in this publication is owned by multiple parties and may not be re-used without the permission of the relevant copyright owner. MTA: avatrombopag and lusutrombopag for treating thrombocytopenia in people with chronic liver disease needing an elective procedure Pre-meeting briefing © NICE 2019.
    [Show full text]
  • Immune Thrombocytopenia in Adults: Modern Approaches to Diagnosis and Treatment
    Published online: 2019-12-12 275 Immune Thrombocytopenia in Adults: Modern Approaches to Diagnosis and Treatment Hanny Al-Samkari, MD1 David J. Kuter, MD, DPhil1 1 Division of Hematology, Massachusetts General Hospital, Harvard Address for correspondence Hanny Al-Samkari, MD, Division of Medical School, Boston, Massachusetts Hematology, Massachusetts General Hospital, Suite 118, Room 112, Zero Emerson Place, Boston, MA 02114 Semin Thromb Hemost 2020;46:275–288. (e-mail: [email protected]). Abstract Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder affecting approximately 1 in 20,000 people. Patients typically present with clinically benign mucocutaneous bleeding, but morbid internal bleeding can occur. Diagnosis remains clinical, possible only after ruling out other causes of thrombocytopenia through history and laboratory testing. Many adult patients do not require treatment. For those requiring intervention, initial treatment of adult ITP is with corticosteroids, intravenous immunoglobulin, or intravenous anti-RhD immune globulin. These agents are rapid- acting but do not result in durable remissions in most patients. No corticosteroid has Keywords demonstrated superiority to others for ITP treatment. Subsequent treatment of adult ► platelets ITP is typically with thrombopoietin receptor agonists (TPO-RAs; romiplostim or ► immune eltrombopag), rituximab, or splenectomy. TPO-RAs are newer agents that offer an thrombocytopenia excellent response rate but may require prolonged treatment. The choice between ► diagnosis subsequent treatments involves consideration of operative risk, risk of asplenia, drug ► treatment side-effects, quality-of-life issues, and financial costs. Given the efficacy of medical ► corticosteroids therapies and the rate of spontaneous remission in the first year after diagnosis, ► intravenous splenectomy is frequently deferred in modern ITP treatment algorithms.
    [Show full text]
  • Hypervitaminosis - an Emerging Pathological Condition
    International Journal of Health Sciences and Research www.ijhsr.org ISSN: 2249-9571 Review Article Hypervitaminosis - An Emerging Pathological Condition J K Roop PG Department of Zoology, JC DAV College (Affiliated to Panjab University, Chandigarh), Dasuya-144205, District Hoshiarpur, Punjab, India ABSTRACT Vitamins are essential organic compounds that are required in small amounts to regulate various metabolic activities in the body. Prolonged and overconsumption of pharmaceutical forms of both water-soluble and fat-soluble vitamins may lead to toxicity and/or hypervitaminosis. Hypervitaminosis is an acute emerging pathological condition of the body due to excess accumulation of any of the vitamins. In case of acute poisoning with vitamin supplements/drugs, emergency assistance is required to detoxify the effects and restore the organization, structure and function of body’s tissues and organs. Sometimes death may occur due to intoxication to liver, kidney and heart. So, to manage any type of hypervitaminosis, proper diagnosis is essential to initiate eliminating the cause of its occurrence and accelerate the elimination of the supplement from the body. The present review discusses the symptoms of hypervitaminosis that seems to be a matter of concern today and management strategies to overcome toxicity or hypervitaminosis. Keywords: Hypervitaminosis, Toxicity, Vitamins, Vitamin pathology, Fat-soluble vitamin, Water- soluble vitamin. INTRODUCTION body, particularly in the liver. Vitamin B Vitamins are potent organic Complex and vitamin C are water- soluble. compounds present in small concentrations They are dissolved easily in food during in various fruits and vegetables. They cooking and a portion of these vitamins may regulate physiological functions and help in be destroyed by heating.
    [Show full text]
  • Relationship Between Digestive Enzymes, Proteins and Anti-Nutritive Factors in Monogastric Digestion
    RELATIONSHIP BETWEEN DIGESTIVE ENZYMES, PROTEINS AND ANTI-NUTRITIVE FACTORS IN MONOGASTRIC DIGESTION By: Theofilos Kempapidis A Thesis Submitted in Partial Fulfilment of the Requirements for the Degree of Doctor of Philosophy Department of Chemical and Biological Engineering Faculty of Engineering The University of Sheffield December 2019 ‘To my beloved mother, whom I couldn’t have done this without and to the memory of my beloved father that passed away during my PhD.’ i ABSTRACT Monogastrics’ lack of some digestive enzymes is compensated by using exogenous enzymes in the animal feed. Those interact with feed ingredients causing enzyme inhibition. Two known inhibiting substances are phytic acid and polyphenolics. Phytase is an important exogenous enzyme that is breaking down phytic acid. The effect of sorghum polyphenolic-rich extracts on the 6-phytase activity was investigated using an ITC by calculating its relative activity. Results show inhibition of the phytase, from all three extracts. For a better understanding of this assay, a real-time mass spectroscopic analysis was performed, that showed the pattern in which the phytase is hydrolysing phytic acid. Consecutively, the effect of phytic acid on the activity of three proteases exogenous and endogenous chymotrypsin and endogenous trypsin was studied. A colorimetric assay using casein as a substrate was used. The results showed different levels of inhibition of all three enzymes by phytic acid. Finally, the interaction between the exogenous chymotrypsin and the phytase was studied by using the ITC enzyme assay and an SDS-Page gel analysis. ITC results showed partial inhibition of the phytase activity, while SDS-Page results showed complete inhibition.
    [Show full text]
  • Essential Trace Elements in Human Health: a Physician's View
    Margarita G. Skalnaya, Anatoly V. Skalny ESSENTIAL TRACE ELEMENTS IN HUMAN HEALTH: A PHYSICIAN'S VIEW Reviewers: Philippe Collery, M.D., Ph.D. Ivan V. Radysh, M.D., Ph.D., D.Sc. Tomsk Publishing House of Tomsk State University 2018 2 Essential trace elements in human health UDK 612:577.1 LBC 52.57 S66 Skalnaya Margarita G., Skalny Anatoly V. S66 Essential trace elements in human health: a physician's view. – Tomsk : Publishing House of Tomsk State University, 2018. – 224 p. ISBN 978-5-94621-683-8 Disturbances in trace element homeostasis may result in the development of pathologic states and diseases. The most characteristic patterns of a modern human being are deficiency of essential and excess of toxic trace elements. Such a deficiency frequently occurs due to insufficient trace element content in diets or increased requirements of an organism. All these changes of trace element homeostasis form an individual trace element portrait of a person. Consequently, impaired balance of every trace element should be analyzed in the view of other patterns of trace element portrait. Only personalized approach to diagnosis can meet these requirements and result in successful treatment. Effective management and timely diagnosis of trace element deficiency and toxicity may occur only in the case of adequate assessment of trace element status of every individual based on recent data on trace element metabolism. Therefore, the most recent basic data on participation of essential trace elements in physiological processes, metabolism, routes and volumes of entering to the body, relation to various diseases, medical applications with a special focus on iron (Fe), copper (Cu), manganese (Mn), zinc (Zn), selenium (Se), iodine (I), cobalt (Co), chromium, and molybdenum (Mo) are reviewed.
    [Show full text]
  • The Practice and Regulatory Requirements Of
    School of Public Health The Practice and Regulatory Requirements of Naturopathy and Western Herbal Medicine Vivian Lin Alan Bensoussan Stephen P. Myers Pauline McCabe Marc Cohen Sophie Hill Genevieve Howse November, 2005 Funded by the Department of Human Services, Victoria Copyright State of Victoria, Department of Human Services, 2006 This publication is copyright. No part may be reproduced by any process except in accordance with the provisions of the Copyright Act 1968 (Cth). Authorised by the State Government of Victoria, 50 Lonsdale Street Melbourne. This document may be downloaded from the following website: www.health.vic.gov.au/pracreg/naturopathy.htm ISBN-13: 978-0-9775864-0-0 ISBN-10: 0-9775864-0-5 Published by School of Public Health, La Trobe University Bundoora Victoria, 3086 Australia THE PRACTICE AND REGULATORY REQUIREMENTS OF NATUROPATHY AND WESTERN HERBAL MEDICINE CONTENTS VOLUME ONE Summary Report..........................................................................................................1 1. Introduction.......................................................................................................1 2. Methodology.....................................................................................................1 3. Key findings and recommendations..................................................................2 3.1 Definition of practice and scope of study ........................................................2 3.2 Growing use of naturopathy and WHM...........................................................3
    [Show full text]
  • Hepatic Pathology in Vitamin a Toxicity FAIRPOUR FOROUHAR, M.D.* MARTIN S
    ANNALS OF CLINICAL AND LABORATORY SCIENCE, Vol. 14, No. 4 Copyright © 1984, Institute for Clinical Science, Inc. Hepatic Pathology in Vitamin A Toxicity FAIRPOUR FOROUHAR, M.D.* MARTIN S. NADEL, M.D.,t and BERNARD GONDOS, M.D.* *Department of Pathology, University of Connecticut, Farmington, CT 06032 and fDepartment of Pathology, Middlesex Memorial Hospital, Middletown, CT 06457 ABSTRACT This paper documents a case of vitamin A toxicity presenting with splenomegaly and ascites. The light microscopic, electron microscopic, and fluorescent findings are described in detail. The principal histopath­ ologic finding was marked perisinusoidal fibrosis. The role of Ito cells in the storage of lipid-soluble vitamins and their subsequent transformation to fibroblasts producing collagen are discussed. tient denied use of medications but admitted long Introduction time use of a self-prescribed vitamin B1-B6 combi­ nation, vitamin B12, iodine, and garlic. Vitamin A Liver disease resulting from vitamin A had been taken for six years, initially 75,000 units toxicity is an uncommon but well docu­ daily, increased to 150,000 units daily two years prior to admission because of believed problems with night mented entity.6’1414’22’26,27 The present vision for which no medical help had been sought. case provides a good model for the study Physical examination disclosed no palpable spleno­ of fibrosis of the space of Disse and its megaly with liver felt one cm beneath the right costal margin. An abdominal fluid wave was present. No pathophysiologic ^consequences. Similar spider angiomata were noted, and the remainder of changes also occur in other conditions re­ the physical examination was unremarkable.
    [Show full text]
  • Metabolomics Identifies Pyrimidine Starvation As the Mechanism of 5-Aminoimidazole-4-Carboxamide-1- Β-Riboside-Induced Apoptosis in Multiple Myeloma Cells
    Published OnlineFirst April 12, 2013; DOI: 10.1158/1535-7163.MCT-12-1042 Molecular Cancer Cancer Therapeutics Insights Therapeutics Metabolomics Identifies Pyrimidine Starvation as the Mechanism of 5-Aminoimidazole-4-Carboxamide-1- b-Riboside-Induced Apoptosis in Multiple Myeloma Cells Carolyne Bardeleben1, Sanjai Sharma1, Joseph R. Reeve3, Sara Bassilian3, Patrick Frost1, Bao Hoang1, Yijiang Shi1, and Alan Lichtenstein1,2 Abstract To investigate the mechanism by which 5-aminoimidazole-4-carboxamide-1-b-riboside (AICAr) induces apoptosis in multiple myeloma cells, we conducted an unbiased metabolomics screen. AICAr had selective effects on nucleotide metabolism, resulting in an increase in purine metabolites and a decrease in pyrimidine metabolites. The most striking abnormality was a 26-fold increase in orotate associated with a decrease in uridine monophosphate (UMP) levels, indicating an inhibition of UMP synthetase (UMPS), the last enzyme in the de novo pyrimidine biosynthetic pathway, which produces UMP from orotate and 5-phosphoribosyl- a-pyrophosphate (PRPP). As all pyrimidine nucleotides can be synthesized from UMP, this suggested that the decrease in UMP would lead to pyrimidine starvation as a possible cause of AICAr-induced apoptosis. Exogenous pyrimidines uridine, cytidine, and thymidine, but not purines adenosine or guanosine, rescued multiple myeloma cells from AICAr-induced apoptosis, supporting this notion. In contrast, exogenous uridine had no protective effect on apoptosis resulting from bortezomib, melphalan, or metformin. Rescue resulting from thymidine add-back indicated apoptosis was induced by limiting DNA synthesis rather than RNA synthesis. DNA replicative stress was identified by associated H2A.X phosphorylation in AICAr-treated cells, which was also prevented by uridine add-back.
    [Show full text]