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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). -
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 ~· ,,;. -
VOLUME 7 2 . No. 4 . AUGUST 2 0
VOLUME 72 . No.4 . AUGUST 2020 © 2020 EDIZIONI MINERVA MEDICA Minerva Pediatrica 2020 August;72(4):288-311 Online version at http://www.minervamedica.it DOI: 10.23736/S0026-4946.20.05861-2 REVIEW MANAGEMENT OF THE MAIN ENDOCRINE AND DIABETIC DISORDERS IN CHILDREN Current treatment for polycystic ovary syndrome: focus on adolescence Maria E. STREET 1 *, Francesca CIRILLO 1, Cecilia CATELLANI 1, 2, Marco DAURIZ 3, 4, Pietro LAZZERONI 1, Chiara SARTORI 1, Paolo MOGHETTI 4 1Division of Pediatric Endocrinology and Diabetology, Department of Mother and Child, Azienda USL – IRCCS di Reggio Emilia, Reggio Emilia, Italy; 2Clinical and Experimental Medicine PhD Program, University of Modena and Reggio Emilia, Modena, Italy; 3Section of Endocrinology and Diabetes, Department of Internal Medicine, Bolzano General Hospital, Bolzano, Italy; 4Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University and Hospital Trust of Verona, Verona, Italy *Corresponding author: Maria E. Street, Division of Pediatric Endocrinology and Diabetology, Department of Mother and Child, Azienda USL – IRCCS di Reggio Emilia, Viale Risorgimento 80, 42123 Reggio Emilia, Italy. E-mail: [email protected] ABSTRACT Polycystic ovary syndrome (PCOS) is the most frequent endocrine disorder in women and it is associated with an in- creased rate of infertility. Its etiology remains largely unknown, although both genetic and environmental factors play a role. PCOS is characterized by insulin resistance, metabolic disorders and low-grade chronic inflammation. To date, the treatment of PCOS is mainly symptomatic and aimed at reducing clinical signs of hyperandrogenism (hirsutism and acne), at improving menstrual cyclicity and at favoring ovulation. Since PCOS pathophysiology is still largely unknown, the therapeutic interventions currently in place are rarely cause-specific. -
Formaldehyde? Formaldehyde Is a Colorless, Strong-Smelling Gas Used to Make Household Products and Building Materials, Furniture, and Paper Products
What is formaldehyde? Formaldehyde is a colorless, strong-smelling gas used to make household products and building materials, furniture, and paper products. It is used in particleboard, plywood, and fiberboard. What products contain formaldehyde? Formaldehyde can be found in most homes and buildings. Formaldehyde is also released into the air from many products you may use in your home. Because formaldehyde breaks down in air, you may breathe it in from such products as • carpet cleaner • gas cookers and open fireplaces, • cosmetics, • glue, • fabric softeners, • household cleaners, and • fingernail polish and hardeners, • latex paint. Burning cigarettes and other tobacco products also release formaldehyde. Products give off different amounts of formaldehyde. For example, • fingernail polish gives off more formaldehyde than do plywood and new carpet, and • some paper products—such as grocery bags and paper towels—give off only small amounts of formaldehyde. Our bodies even produce some formaldehyde, although only in small amounts. Will I get sick if I breathe or touch formaldehyde? You might not get sick if you breathe or touch formaldehyde, but if you have breathed or touched formaldehyde you may have symptoms such as • sore, itchy, or burning eyes, nose, or throat; • skin rash; or • breathing symptoms such as chest tightness, coughing, and shortness of breath. People who are more likely to get sick from being around formaldehyde are children, the elderly, and people with asthma. Formaldehyde may affect children more than it does adults. If you think your child may have been around formaldehyde, and he or she has symptoms contact a doctor. You should also know that: babies are not likely to get formaldehyde from breast milk, and you may be more sensitive to formaldehyde if you have asthma. -
Method 323—Measurement of Formaldehyde Emissions from Natural Gas-Fired Stationary Sources—Acetyl Acetone Derivitization Method
While we have taken steps to ensure the accuracy of this Internet version of the document, it is not the official version. Please refer to the official version in the FR publication, which appears on the Government Printing Office's FDSys website (http://www.gpo.gov/fdsys/browse/collectionCfr.action?). Method 323—Measurement of Formaldehyde Emissions From Natural Gas-Fired Stationary Sources—Acetyl Acetone Derivitization Method 1.0 Introduction. This method describes the sampling and analysis procedures of the acetyl acetone colorimetric method for measuring formaldehyde emissions in the exhaust of natural gas-fired, stationary combustion sources. This method, which was prepared by the Gas Research Institute (GRI), is based on the Chilled Impinger Train Method for Methanol, Acetone, Acetaldehyde, Methyl Ethyl Ketone, and Formaldehyde (Technical Bulletin No. 684) developed and published by the National Council of the Paper Industry for Air and Stream Improvement, Inc. (NCASI). However, this method has been prepared specifically for formaldehyde and does not include specifications (e.g., equipment and supplies) and procedures (e.g., sampling and analytical) for methanol, acetone, acetaldehyde, and methyl ethyl ketone. To obtain reliable results, persons using this method should have a thorough knowledge of at least Methods 1 and 2 of 40 CFR part 60, appendix A–1; Method 3 of 40 CFR part 60, appendix A–2; and Method 4 of 40 CFR part 60, appendix A–3. 1.1 Scope and Application 1.1.1 Analytes. The only analyte measured by this method is formaldehyde (CAS Number 50–00–0). 1.1.2 Applicability. This method is for analyzing formaldehyde emissions from uncontrolled and controlled natural gas-fired, stationary combustion sources. -
Study Protocol and Statistical Analysis Plan
Confidential Clinical study protocol number: J1228 Page 1 Version Date: May 7, 2018 IRB study Number: NA_00067315 A Trial of maintenance Rituximab with mTor inhibition after High-dose Consolidative Therapy in CD20+, B-cell Lymphomas, Gray Zone Lymphoma, and Hodgkin’s Lymphoma Principal Investigator: Douglas E. Gladstone, MD The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins 1650 Orleans Street, CRBI-287 Baltimore, MD 21287 Phone: 410-955-8781 Fax: 410-614-1005 Email: [email protected] IRB Protocol Number: NA_00067315 Study Number: J1228 IND Number: EXEMPT Novartis Protocol Number: CRAD001NUS157T Version: May 7, 2018 Co-Investigators: Jonathan Powell 1650 Orleans Street, CRBI-443 Phone: 410-502-7887 Fax: 443-287-4653 Email: [email protected] Richard Jones 1650 Orleans Street, CRBI-244 Phone: 410-955-2006 Fax: 410-614-7279 Email: [email protected] Confidential Clinical study protocol number: J1228 Page 2 Version Date: May 7, 2018 IRB study Number: NA_00067315 Satish Shanbhag Johns Hopkins Bayview Medical Center 301 Building, Suite 4500 4940 Eastern Ave Phone: 410-550-4061 Fax: 410-550-5445 Email: [email protected] Statisticians: Gary Rosner Phone: 410-955-4884 Email: [email protected] Marianna Zahurak Phone: 410-955-4219 Email: [email protected] Confidential Clinical study protocol number: J1228 Page 3 Version Date: May 7, 2018 IRB study Number: NA_00067315 Table of contents Table of contents ......................................................................................................................... 3 List of abbreviations -
Toxicological Profile for Formaldehyde
TOXICOLOGICAL PROFILE FOR FORMALDEHYDE U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service Agency for Toxic Substances and Disease Registry July 1999 FORMALDEHYDE ii DISCLAIMER The use of company or product name(s) is for identification only and does not imply endorsement by the Agency for Toxic Substances and Disease Registry. FORMALDEHYDE iii UPDATE STATEMENT Toxicological profiles are revised and republished as necessary, but no less than once every three years. For information regarding the update status of previously released profiles, contact ATSDR at: Agency for Toxic Substances and Disease Registry Division of Toxicology/Toxicology Information Branch 1600 Clifton Road NE, E-29 Atlanta, Georgia 30333 FORMALDEHYDE vii QUICK REFERENCE FOR HEALTH CARE PROVIDERS Toxicological Profiles are a unique compilation of toxicological information on a given hazardous substance. Each profile reflects a comprehensive and extensive evaluation, summary, and interpretation of available toxicologic and epidemiologic information on a substance. Health care providers treating patients potentially exposed to hazardous substances will find the following information helpful for fast answers to often-asked questions. Primary Chapters/Sections of Interest Chapter 1: Public Health Statement: The Public Health Statement can be a useful tool for educating patients about possible exposure to a hazardous substance. It explains a substance’s relevant toxicologic properties in a nontechnical, question-and-answer format, and it includes a review of the general health effects observed following exposure. Chapter 2: Health Effects: Specific health effects of a given hazardous compound are reported by route of exposure, by type of health effect (death, systemic, immunologic, reproductive), and by length of exposure (acute, intermediate, and chronic). -
The Decomposition Kinetics of Peracetic Acid and Hydrogen Peroxide in Municipal Wastewaters
Disinfection Forum No 10, October 2015 The Decomposition Kinetics of Peracetic Acid and Hydrogen Peroxide in Municipal Wastewaters INTRODUCTION Efficient control of microbial populations in municipal wastewater using peracetic acid (PAA) requires an understanding of the PAA decomposition kinetics. This knowledge is critical to ensure the proper dosing of PAA needed to achieve an adequate concentration within the contact time of the disinfection chamber. In addition, the impact of PAA on the environment, post-discharge into the receiving water body, also is dependent upon the longevity of the PAA in the environment, before decomposing to acetic acid, oxygen and water. As a result, the decomposition kinetics of PAA may have a significant impact on aquatic and environmental toxicity. PAA is not manufactured as a pure compound. The solution exists as an equilibrium mixture of PAA, hydrogen peroxide, acetic acid, and water: ↔ + + Acetic Acid Hydrogen Peroxide Peracetic Acid Water PeroxyChem’s VigorOx® WWT II Wastewater Disinfection Technology contains 15% peracetic acid by weight and 23% hydrogen peroxide as delivered. Although hydrogen peroxide is present in the formulation, peracetic acid is considered to be the active component for disinfection1 in wastewater. There have been several published studies investigating the decomposition kinetics of PAA in different water matrices, including municipal wastewater2-7. Yuan7 states that PAA may be consumed in the following three competitive reactions: 1. Spontaneous decomposition 2 CH3CO3H à 2 CH3CO2H + O2 Eq (1) 2. Hydrolysis CH3CO3H + H2O à CH3CO2H + H2O2 Eq (2) 3. Transition metal catalyzed decomposition + CH3CO3H + M à CH3CO2H + O2 + other products Eq (3) At neutral pH’s, both peracetic acid and hydrogen peroxide can be rapidly consumed by these reactions7 (hydrogen peroxide will decompose to water and oxygen via 2H2O2 à 2H2O + O2). -
Opposing Effects of Dehydroepiandrosterone And
European Journal of Endocrinology (2000) 143 687±695 ISSN 0804-4643 EXPERIMENTAL STUDY Opposing effects of dehydroepiandrosterone and dexamethasone on the generation of monocyte-derived dendritic cells M O Canning, K Grotenhuis, H J de Wit and H A Drexhage Department of Immunology, Erasmus University Rotterdam, The Netherlands (Correspondence should be addressed to H A Drexhage, Lab Ee 838, Department of Immunology, Erasmus University, PO Box 1738, 3000 DR Rotterdam, The Netherlands; Email: [email protected]) Abstract Background: Dehydroepiandrosterone (DHEA) has been suggested as an immunostimulating steroid hormone, of which the effects on the development of dendritic cells (DC) are unknown. The effects of DHEA often oppose those of the other adrenal glucocorticoid, cortisol. Glucocorticoids (GC) are known to suppress the immune response at different levels and have recently been shown to modulate the development of DC, thereby influencing the initiation of the immune response. Variations in the duration of exposure to, and doses of, GC (particularly dexamethasone (DEX)) however, have resulted in conflicting effects on DC development. Aim: In this study, we describe the effects of a continuous high level of exposure to the adrenal steroid DHEA (1026 M) on the generation of immature DC from monocytes, as well as the effects of the opposing steroid DEX on this development. Results: The continuous presence of DHEA (1026 M) in GM-CSF/IL-4-induced monocyte-derived DC cultures resulted in immature DC with a morphology and functional capabilities similar to those of typical immature DC (T cell stimulation, IL-12/IL-10 production), but with a slightly altered phenotype of increased CD80 and decreased CD43 expression (markers of maturity). -
Triclosan Disrupts Thyroid Hormones: Mode-Of-Action, Developmental Susceptibility, and Determination of Human Relevance
Triclosan Disrupts Thyroid Hormones: Mode-of-Action, Developmental Susceptibility, and Determination of Human Relevance Katie Beth Paul “A dissertation submitted to the faculty of the University of North Carolina at Chapel Hill in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Curriculum of Toxicology.” Chapel Hill 2011 Approved by: Kim L. R. Brouwer, Pharm.D., Ph.D. Kevin M. Crofton, Ph.D. Michael J. DeVito, Ph.D. Philip C. Smith, Ph.D James A. Swenberg, D.V.M., Ph.D. ©2011 Katie Beth Paul ALL RIGHTS RESERVED ii Abstract Katie Beth Paul Triclosan Disrupts Thyroid Hormones: Mode-of-Action, Developmental Susceptibility, and Determination of Human Relevance (Under the direction of Kevin M. Crofton, Ph.D.) Preliminary study demonstrated that triclosan (TCS), a bacteriostat in myriad consumer products, decreases serum thyroxine (T4) in rats. Adverse neurodevelopmental consequences result from thyroid hormone (TH) disruption; therefore determination of whether TCS disrupts THs during development, its mode-of-action (MOA), and the human relevance is critical. This research tested the hypothesis that TCS disrupts THs via activation of pregnane X and constitutive androstane receptors (PXR, CAR), mediating Phase I-II enzyme and hepatic transporter expression and protein changes, thereby increasing catabolism and elimination of THs, resulting in decreased TH concentrations. For Aim One, the hypothesized MOA was assessed using weanling female Long-Evans rats orally exposed to TCS (0-1000 mg/kg/day) for four days. Serum T4 decreased 35% at 300 mg/kg/day. Activity and expression of markers of Phase I (Cyp2b, Cyp3a1) and Phase II (Ugt1a1, Sult1c1) metabolism were moderately induced, consistent with PXR and/or CAR activation and increased hepatic catabolism. -
University of Groningen Discovery of a Eugenol Oxidase From
University of Groningen Discovery of a eugenol oxidase from Rhodococcus sp strain RHA1 Jin, J.F.; Mazon, H.; van den Heuvel, R.H.H.; Janssen, D.B.; Fraaije, M.W. Published in: Febs Journal DOI: 10.1111/j.1742-4658.2007.05767.x IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below. Document Version Publisher's PDF, also known as Version of record Publication date: 2007 Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Jin, J. F., Mazon, H., van den Heuvel, R. H. H., Janssen, D. B., & Fraaije, M. W. (2007). Discovery of a eugenol oxidase from Rhodococcus sp strain RHA1. Febs Journal, 274(9), 2311 - 2321. https://doi.org/10.1111/j.1742-4658.2007.05767.x Copyright Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons). Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. Download date: 23-09-2021 Discovery of a eugenol oxidase from Rhodococcus sp. -
An Open-Label Pilot Trial of Alpha-Lipoic Acid for Weight Loss in Patients with Schizophrenia Without Diabetes Joseph C
Case Reports An Open-Label Pilot Trial of Alpha-Lipoic Acid for Weight Loss in Patients with Schizophrenia without Diabetes Joseph C. Ratliff1 , Laura B. Palmese 1, Erin L. Reutenauer 1, Cenk Tek 1 Abstract A possible mechanism of antipsychotic-induced weight gain is activation of hypothalamic monophosphate-dependent kinase (AMPK) mediated by histamine 1 receptors. Alpha-lipoic acid (ALA), a potent antioxidant, counteracts this ef- fect and may be helpful in reducing weight for patients taking antipsychotics. The objective of this open-label study was to assess the efficacy of ALA (1,200 mg) on twelve non-diabetic schizophrenia patients over ten weeks. Participants lost significant weight during the intervention (-2.2 kg±2.5 kg). ALA was well tolerated and was particularly effective for individuals taking strongly antihistaminic antipsychotics (-2.9 kg±2.6 kg vs. -0.5 kg±1.0 kg). Clinical Trial Registra- tion: NCT01355952. Key Words: Schizophrenia, Obesity, Schizoaffective Disorder, Alpha-Lipoic Acid Introduction dependent protein kinase (AMPK) in the hypothalamus Antipsychotic medications appear to induce weight (4). In the periphery, AMPK increases energy utilization; gain, which results in increased rates of obesity in schizo- AMPK activity in the hypothalamus increases appetite. phrenia (1). Schizophrenia patients have significantly short- Several highly orexigenic (stimulates appetite) antipsy- er life expectancy than the general population (2); most of chotics such as clozapine, olanzapine, and quetiapine are this excess mortality is attributed to diabetes and cardiovas- shown to activate AMPK in the hypothalamus in animal cular disease (3); weight gain is a significant contributor to studies whereas other antipsychotic medications do not (4).