Psychiatric Implications of Nutritional Deficiencies in Alcoholism
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Magnesium Causes Nitric Oxide Independent Coronary Artery Vasodilation in Humans Heart: First Published As 10.1136/Hrt.86.2.212 on 1 August 2001
212 Heart 2001;86:212–216 Magnesium causes nitric oxide independent coronary artery vasodilation in humans Heart: first published as 10.1136/hrt.86.2.212 on 1 August 2001. Downloaded from H Teragawa, M Kato, T Yamagata, H Matsuura, G Kajiyama Abstract Objective—To determine how magnesium aVects human coronary arteries and whether endothe- lium derived nitric oxide (EDNO) is involved in the coronary arterial response to magnesium. Design—Quantitative coronary angiography and Doppler flow velocity measurements were used to determine the eVects of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) on magnesium induced dilation of the epicardial and resistance coronary arteries. Setting—Hiroshima University Hospital a tertiary cardiology centre. Patients—17 patients with angiographically normal coronary arteries. Interventions—Magnesium sulfate (MgSO4) (0.02 mmol/min and 0.2 mmol/min) was infused for two minutes into the left coronary ostium before and after intracoronary infusion of L-NMMA. Main outcome measures—Diameter of the proximal and distal segments of the epicardial cor- onary arteries and coronary blood flow. Results—At a dose of 0.02 mmol/min, MgSO4 did not aVect the coronary arteries. At a dose of 0.2 mmol/min, MgSO4 caused coronary artery dilation (mean (SEM) proximal diameter 3.00 (0.09) to 3.11 (0.09) mm; distal 1.64 (0.06) to 1.77 (0.07) mm) and increased coronary blood flow (79.3 (7.5) to 101.4 (9.9) ml/min, p < 0.001 v baseline for all). MgSO4 increased the changes in these parameters after the infusion of L-NMMA (p < 0.001 v baseline). -
Recent Insights Into the Role of Vitamin B12 and Vitamin D Upon Cardiovascular Mortality: a Systematic Review
Acta Scientific Pharmaceutical Sciences (ISSN: 2581-5423) Volume 2 Issue 12 December 2018 Review Article Recent Insights into the Role of Vitamin B12 and Vitamin D upon Cardiovascular Mortality: A Systematic Review Raja Chakraverty1 and Pranabesh Chakraborty2* 1Assistant Professor, Bengal School of Technology (A College of Pharmacy), Sugandha, Hooghly, West Bengal, India 2Director (Academic), Bengal School of Technology (A College of Pharmacy),Sugandha, Hooghly, West Bengal, India *Corresponding Author: Pranabesh Chakraborty, Director (Academic), Bengal School of Technology (A College of Pharmacy), Sugandha, Hooghly, West Bengal, India. Received: October 17, 2018; Published: November 22, 2018 Abstract since the pathogenesis of several chronic diseases have been attributed to low concentrations of this vitamin. The present study Vitamin B12 and Vitamin D insufficiency has been observed worldwide at all stages of life. It is a major public health problem, throws light on the causal association of Vitamin B12 to cardiovascular disorders. Several evidences suggested that vitamin D has an effect in cardiovascular diseases thereby reducing the risk. It may happen in case of gene regulation and gene expression the vitamin D receptors in various cells helps in regulation of blood pressure (through renin-angiotensin system), and henceforth modulating the cell growth and proliferation which includes vascular smooth muscle cells and cardiomyocytes functioning. The present review article is based on identifying correct mechanisms and relationships between Vitamin D and such diseases that could be important in future understanding in patient and healthcare policies. There is some reported literature about the causative association between disease (CAD). Numerous retrospective and prospective studies have revealed a consistent, independent relationship of mild hyper- Vitamin B12 deficiency and homocysteinemia, or its role in the development of atherosclerosis and other groups of Coronary artery homocysteinemia with cardiovascular disease and all-cause mortality. -
THE ACCUMULATION and DISTRIBUTION of EVANS BLUE in the KIDNEY of RATS FED NORMAL OR LOW MAGNESIUM DIETS by George Williams Seign
THE ACCUMULATION AND DISTRIBUTION OF EVANS BLUE IN THE KIDNEY OF RATS FED NORMAL OR LOW MAGNESIUM DIETS by George Williams Seignious, IV Thesis submitted to the Graduate Faculty of the Virginia Polytechnic Institute and State University in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE in ! Biochemistry and Nutrition APPROVED: G. E. Bunce, Chairman R. E. Webb ______ fl" ________ M;O. ......... ..;:;...; ___'"";:,....:; __.;..,. ___ _ _.. ''-.::;,,/ ___ , _______ ,_.._~_ M. H. Samli R. G. Saacke August, 1973 Blacksburg, Virginia . l\CKNOWLEDGMEN',rS The author of this thesis would like to e~press his deepest thanks and gra'titU;de to for his.continued help, advice, and . ·. .. : .. - understanding which made this thesis possible •. A special note of ·"· thanks is expressed.to whos_e invaluable help, advice arid suggestions aided greatly the author's efforts. The author would also like to thank for his. help and advice in the lab and all the other graduate students who made the author's stay at Virginia.Tech i{ very pleasant _one. Thanks is expressed to the author's wife, , for .her love, understanding, encouragement, and typing which· enabled the completion of this thesis. Also the author would like.to thank his parents for their lc;rving support and financial assistance. ii 'TABLE OF CONTENTS ACKNOWLEDGMENTS ii. TABLE OF CONTENTS . iii I,.IST OF TABLES iv LIST OF FIGURES Vi LIST OF SELECTED CHEMICAL STRUCTURES vii LIST OF·ABBREVIATIONS viii INTRODUCTION 1 LITERATURE REVIEW 5 EXPERIMENTAL PROCEDURES RESULTS 33 DISCUSSION 74 SUMMARY 82 REFERENCES 85 VITA 88 iii ~· ,,;. -
Polymorphisms in Folic Acid Metabolism Genes Do Not Associate with Cancer Cachexia in Japanese Gastrointestinal Patients
ORIGINAL PAPER Nagoya J. Med. Sci. 80. 529–539, 2018 doi:10.18999/nagjms.80.4.529 Polymorphisms in folic acid metabolism genes do not associate with cancer cachexia in Japanese gastrointestinal patients Takuto Morishita1, Asahi Hishida1, Yoshinaga Okugawa2,3,6, Yuuki Morimoto2, Yumiko Shirai4, Kyoko Okamoto5, Sachiko Momokita6, Aki Ogawa5, Koji Tanaka2,7, Ryutaro Nishikawa2, Yuji Toiyama7, Yasuhiro Inoue7, Hiroyuki Sakurai8, Hisashi Urata2, Motoyoshi Tanaka3, and Chikao Miki2,7 1Department of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan 2Departments of Surgery, Iga City General Hospital, Iga, Japan 3Departments of Medical Oncology, Iga City General Hospital, Iga, Japan 4Departments of Nutrition, Iga City General Hospital, Iga, Japan 5Departments of Nursing, Iga City General Hospital, Iga, Japan 6Departments of Biochemical Laboratory, Iga City General Hospital, Iga, Japan 7Department of Gastrointestinal and Pediatric Surgery, Division of Reparative Medicine, Institute of Life Sciences, Mie University Graduate School of Medicine, Tsu, Japan 8Department of Hepatobiliary Pancreatic and Transplant Surgery, Mie University Graduate School of Medicine, Tsu, Japan. ABSTRACT We used clinical data from Iga General Hospital to examine the association between polymorphisms in MTR (methionine synthase) A2756G (rs1805087), MTRR (methionine synthase reductase) His595Tyr (rs10380), MTHFR (methylenetetrahydrofolate reductase) C677T (rs1801133), MTHFR A1298C (rs1801131) and SHMT (serine hydroxymethyltransferase) C1420T (rs1979277), which are genes involved in folate metabolism, and the risk of weight loss in patients with gastrointestinal cancers, with the aim of establishing personalized palliative care for each patient based on genetic information. The data from 59 patients (37 males and 22 females) with gastrointestinal cancers who visited the outpatient clinic for cancer chemotherapy and palliative care at Iga General Hospital from December 2011 to August 2015 were analyzed. -
Magnesium Production
Magnesium Production Subpart T, Greenhouse Gas Reporting Program Under the Greenhouse Gas Reporting Program (GHGRP), owners or operators of facilities that contain magnesium production processes must report emissions from use of cover and carrier gases as well as for all other source categories located at the facility for which methods are defined in the rule. Owners and operators are required to collect emission data, calculate greenhouse gas (GHG) emissions and follow the specified procedures for quality assurance, missing data, recordkeeping, and reporting per the requirements of 40 CFR Part 98 Subpart T – Magnesium Production. How Is This Source Category Defined? The magnesium production source category is defined as consisting of any process where magnesium metal is produced through smelting (including electrolytic smelting), refining, or remelting operations (including primary production facilities that extract magnesium from its ore and secondary production facilities that recover magnesium from scrap), or any process where molten magnesium is used in alloying, casting, drawing, extruding, forming, or rolling operations. Who Must Report? Magnesium production facilities that emit more than 25,000 metric tons CO2e per year. What Greenhouse Gases Must Be Reported? Each facility must report total annual emissions for each of the following greenhouse gases used in magnesium production facilities: ● Sulfur hexafluoride (SF6) ● HFC-134a ● The fluorinated ketone FK 5-1-12 ● Carbon dioxide (CO2) ● Any other GHG as defined in 40 CFR part 98, subpart A (General Provisions) of the rule In addition, the facility must report greenhouse gas emissions for any other source categories for which calculation methods are provided in the rule, as applicable. -
Family Practice
THE JOURNAL OF FAMILY PRACTICE Emmanuel Andrès, MD, B12 deficiency: A look beyond Laure Federici, MD, Stéphan Affenberger, MD pernicious anemia Department of Internal Medicine, Diabetes and Metabolic Diseases, Food-B12 malabsorption—not pernicious anemia—is the Hôpitaux Universitaires de Strasbourg, leading cause of B12 malabsorption. It’s also very subtle Strasbourg, France emmanuel.andres @chru-strasbourg.fr Practice recommendations such as its link to Helicobacter pylori • Mild, preclinical B deficiency infection and long-term antacid and bi- Josep Vidal-Alaball, MD 12 Department of General is associated with food-B12 guanide use. It also requires that you Practice, Cardiff University, malabsorption more often than consider not only a patient’s serum B12 United Kingdom with pernicious anemia. (C) ® Dowdenlevels, but his Health homocysteine Media and meth - Noureddine Henoun ylmalonic acid levels, since they are con- Loukili, PhD • The classic treatment for B 12 Department of Hygiene and deficiency—particularly when the sidered more sensitive indicators of co- 6 Fight against Nosocomial cause is not a dietaryCopyright deficiency—isFor personalbalamin deficiency. use Keyingonly in on these Infections, Hôpital Calmette, 100 to 1000 mcg per month of indicators early will ensure prompt treat- CHRU de Lille, Lille, France cyanocobalamin, IM. (B) ment, which typically includes intramus- cular injections of the vitamin, but which Jacques Zimmer, MD, PhD • Oral crystalline cyanocobalamin could revolve around a more convenient Laboratoire is an effective treatment for food- d’Immunogénétique- option: oral B12. Allergologie, Centre de B12 malabsorption, though it’s Recherche Public de la Santé effectiveness in the long term has (CRP-Santé) de Luxembourg, not been demonstrated. -
Nutrition 102 – Class 3
Nutrition 102 – Class 3 Angel Woolever, RD, CD 1 Nutrition 102 “Introduction to Human Nutrition” second edition Edited by Michael J. Gibney, Susan A. Lanham-New, Aedin Cassidy, and Hester H. Vorster May be purchased online but is not required for the class. 2 Technical Difficulties Contact: Erin Deichman 574.753.1706 [email protected] 3 Questions You may raise your hand and type your question. All questions will be answered at the end of the webinar to save time. 4 Review from Last Week Vitamins E, K, and C What it is Source Function Requirement Absorption Deficiency Toxicity Non-essential compounds Bioflavonoids: Carnitine, Choline, Inositol, Taurine, and Ubiquinone Phytoceuticals 5 Priorities for Today’s Session B Vitamins What they are Source Function Requirement Absorption Deficiency Toxicity 6 7 What Is Vitamin B1 First B Vitamin to be discovered 8 Vitamin B1 Sources Pork – rich source Potatoes Whole-grain cereals Meat Fish 9 Functions of Vitamin B1 Converts carbohydrates into glucose for energy metabolism Strengthens immune system Improves body’s ability to withstand stressful conditions 10 Thiamine Requirements Groups: RDA (mg/day): Infants 0.4 Children 0.7-1.2 Males 1.5 Females 1 Pregnancy 2 Lactation 2 11 Thiamine Absorption Absorbed in the duodenum and proximal jejunum Alcoholics are especially susceptible to thiamine deficiency Excreted in urine, diuresis, and sweat Little storage of thiamine in the body 12 Barriers to Thiamine Absorption Lost into cooking water Unstable to light Exposure to sunlight Destroyed -
Case Study 54 Year Old Female with DEPRESSION
Case Study 54 year old female with DEPRESSION Patient was initially seen in June of 2008. She had been suffering from depression for the past 5 years. Her psychiatrist had tried various anti-depressant medications, including Zoloft and Lexapro. At the time of her initial consultation, she was taking Prozac which provided mild relief of her depression. In addition to this, she had been taking Prempro for 3 years. Interestingly, her homocysteine levels were 18.2 umol/L. She had been taking a once-a-day multivitamin and a calcium citrate/vitamin D supplement. She was 20 pounds overweight. Her appetite was described as “too good”. She also has had a long history of poor sleep. SpectraCell’s MicroNutrient testing revealed functional deficiencies of folic acid, vitamin b6, vitamin d, selenium and serine. However, the whole family of B vitamins was at the lowest end of normal. Based upon these deficiencies, she was administered the following daily nutritional supplement protocol. 1) B-complex weighted with extra B6 (250 mg). This contained 800 mcg of folic acid 2) 1000 IU of vitamin D3. This was in addition to her calcium/vitamin D supplement which provided 400 IU per day 3) 200 mcg of selenium 4) 100 mg of PHOSPHATIDYLSERINE TID In addition, she was instructed to consume foods high in these nutrients. She was also instructed to receive 15 minutes of direct sunlight each morning. Follow up SpectraCell’s MicroNutrient testing was performed six months later. All deficiencies were resolved except for vitamin D, which was improved but not fully resolved. -
Vitamin and Mineral Requirements in Human Nutrition
P000i-00xx 3/12/05 8:54 PM Page i Vitamin and mineral requirements in human nutrition Second edition VITPR 3/12/05 16:50 Page ii WHO Library Cataloguing-in-Publication Data Joint FAO/WHO Expert Consultation on Human Vitamin and Mineral Requirements (1998 : Bangkok, Thailand). Vitamin and mineral requirements in human nutrition : report of a joint FAO/WHO expert consultation, Bangkok, Thailand, 21–30 September 1998. 1.Vitamins — standards 2.Micronutrients — standards 3.Trace elements — standards 4.Deficiency diseases — diet therapy 5.Nutritional requirements I.Title. ISBN 92 4 154612 3 (LC/NLM Classification: QU 145) © World Health Organization and Food and Agriculture Organization of the United Nations 2004 All rights reserved. Publications of the World Health Organization can be obtained from Market- ing and Dissemination, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel: +41 22 791 2476; fax: +41 22 791 4857; e-mail: [email protected]). Requests for permis- sion to reproduce or translate WHO publications — whether for sale or for noncommercial distri- bution — should be addressed to Publications, at the above address (fax: +41 22 791 4806; e-mail: [email protected]), or to Chief, Publishing and Multimedia Service, Information Division, Food and Agriculture Organization of the United Nations, 00100 Rome, Italy. The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization and the Food and Agriculture Organization of the United Nations concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. -
341 Nutrient Deficiency Or Disease Definition/Cut-Off Value
10/2019 341 Nutrient Deficiency or Disease Definition/Cut-off Value Any currently treated or untreated nutrient deficiency or disease. These include, but are not limited to, Protein Energy Malnutrition, Scurvy, Rickets, Beriberi, Hypocalcemia, Osteomalacia, Vitamin K Deficiency, Pellagra, Xerophthalmia, and Iron Deficiency. Presence of condition diagnosed, documented, or reported by a physician or someone working under a physician’s orders, or as self-reported by applicant/participant/caregiver. See Clarification for more information about self-reporting a diagnosis. Participant Category and Priority Level Category Priority Pregnant Women 1 Breastfeeding Women 1 Non-Breastfeeding Women 6 Infants 1 Children 3 Justification Nutrient deficiencies or diseases can be the result of poor nutritional intake, chronic health conditions, acute health conditions, medications, altered nutrient metabolism, or a combination of these factors, and can impact the levels of both macronutrients and micronutrients in the body. They can lead to alterations in energy metabolism, immune function, cognitive function, bone formation, and/or muscle function, as well as growth and development if the deficiency is present during fetal development and early childhood. The Centers for Disease Control and Prevention (CDC) estimates that less than 10% of the United States population has nutrient deficiencies; however, nutrient deficiencies vary by age, gender, and/or race and ethnicity (1). For certain segments of the population, nutrient deficiencies may be as high as one third of the population (1). Intake patterns of individuals can lead to nutrient inadequacy or nutrient deficiencies among the general population. Intakes of nutrients that are routinely below the Dietary Reference Intakes (DRI) can lead to a decrease in how much of the nutrient is stored in the body and how much is available for biological functions. -
Criminal Justice Review 2010/11
Centre for Criminal Justice Studies SCHOOL OF LAW Criminal Justice Review Twenty Third Annual Report 2010/11 Centre for Criminal Justice Studies CRIMINAL JUSTICE REVIEW 2010/11 Twenty Third Annual Report CONTENTS The Centre for Criminal Justice Studies ...................................................................................................... 1 Introduction .................................................................................................................................................... 3 Research Projects ............................................................................................................................................ 5 Security and Justice Research Group: Building Sustainable Societies Transformation Fund ............. 9 Teaching Related Initiatives ........................................................................................................................ 10 The Innocence Project: Enhancing Student Experience and Investigating Wrongful Conviction .......................................................................................................................................... 10 HMP Leeds ......................................................................................................................................... 13 Publications ................................................................................................................................................... 15 Conference Presentations and Public Seminars ...................................................................................... -
Magnesium Deficiency: a Possible Cause of Thiamine Refractoriness in Wernicke-Korsakoff Encephalopathy
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.37.8.959 on 1 August 1974. Downloaded from Journal of Neurology, Neurosurgery, and Psychiatry, 1974, 37, 959-962 Magnesium deficiency: a possible cause of thiamine refractoriness in Wernicke-Korsakoff encephalopathy D. C. TRAVIESA From the Department ofNeurology, University ofMiami School of Medicine, Miami, Florida, U.S.A. SYNOPSIS The determination of blood transketolase before and serially after thiamine administra- tion, and the response of clinical symptomatology after thiamine are reported in two normo- magnesaemic patients and one hypomagnesaemic patient with acute Wernicke-Korsakoff encephalopathy. The response of the depressed blood transketolase and the clinical symptoms was retarded in the hypomagnesaemic patient. Correction of hypomagnesaemia was accompanied by the recovery of blood transketolase activity and total clearing of the ophthalmoplegia in this patient, guest. Protected by copyright. suggesting that hypomagnesaemia may be a cause of the occasional thiamine refractoriness of these patients. Previous studies have shown that the clinical vestibular nuclei (Prickett, 1934; Dreyfus and entity of Wernicke-Korsakoff encephalopathy is Victor, 1961; Dreyfus, 1965). related to an exclusive deficiency of thiamine (Phillips et al., 1952). Furthermore, improvement Blood transketolase activity is markedly re- in clinical symptoms, once the syndrome has de- duced in patients with Wernicke-Korsakoff veloped, occurs only with the repletion of thi- encephalopathy and serial assays in these patients amine. It is this obvious and seemingly pure usually reveal a rapid and essentially complete causal relationship of thiamine deficiency and recovery of the reduced blood transketolase Wernicke-Korsakoff encephalopathy that neces- activity after the parental administration of sitates the total understanding of thiamine thiamine (Brin, 1962; Dreyfus, 1962).