Oecd Guideline for the Testing of Chemicals
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Virulence and Transcriptome Profile of Multidrug-Resistant Escherichia Coli from Chicken Received: 3 April 2017 Hafiz I.Hussain 1, Zahid Iqbal1,4, Mohamed N
www.nature.com/scientificreports OPEN Virulence and transcriptome profile of multidrug-resistant Escherichia coli from chicken Received: 3 April 2017 Hafiz I.Hussain 1, Zahid Iqbal1,4, Mohamed N. Seleem3, Deyu Huang2, Adeel Sattar2, Haihong Accepted: 3 July 2017 Hao1 & Zonghui Yuan1,2 Published: xx xx xxxx Numerous studies have examined the prevalence of pathogenic Escherichia coli in poultry and poultry products; however, limited data are available regarding their resistance- and virulence-associated gene expression profiles. This study was designed to examine the resistance and virulence of poultryE. coli strains in vitro and in vivo via antibiotic susceptibility, biofilm formation and adhesion, and invasion and intracellular survivability assays in Caco-2 and Raw 264.7 cell lines as well as the determination of the median lethal dose in two-day old chickens. A clinical pathogenic multidrug-resistant isolate, E. coli 381, isolated from broilers, was found to be highly virulent in cell culture and 1000-fold more virulent in a chicken model than other strains; accordingly, the isolate was subsequently selected for transcriptome analysis. The comparative gene expression profile of MDRE. coli 381 and the reference human strain E. coli ATCC 25922 was completed with Illumina HiSeq. 2500 transcriptome analysis. Differential gene expression analysis indicates that there are multiple pathways involved in the resistance and virulence of this highly virulent strain. The results garnered from this study provide critical information about the highly virulent MDR E. coli strain of poultry origin and warrant further investigation due to its significant threat to public health. Escherichia coli is a Gram-negative bacterium that displays a wide range of genomic diversity. -
Toxicological Profile for Radon
RADON 205 10. GLOSSARY Some terms in this glossary are generic and may not be used in this profile. Absorbed Dose, Chemical—The amount of a substance that is either absorbed into the body or placed in contact with the skin. For oral or inhalation routes, this is normally the product of the intake quantity and the uptake fraction divided by the body weight and, if appropriate, the time, expressed as mg/kg for a single intake or mg/kg/day for multiple intakes. For dermal exposure, this is the amount of material applied to the skin, and is normally divided by the body mass and expressed as mg/kg. Absorbed Dose, Radiation—The mean energy imparted to the irradiated medium, per unit mass, by ionizing radiation. Units: rad (rad), gray (Gy). Absorbed Fraction—A term used in internal dosimetry. It is that fraction of the photon energy (emitted within a specified volume of material) which is absorbed by the volume. The absorbed fraction depends on the source distribution, the photon energy, and the size, shape and composition of the volume. Absorption—The process by which a chemical penetrates the exchange boundaries of an organism after contact, or the process by which radiation imparts some or all of its energy to any material through which it passes. Self-Absorption—Absorption of radiation (emitted by radioactive atoms) by the material in which the atoms are located; in particular, the absorption of radiation within a sample being assayed. Absorption Coefficient—Fractional absorption of the energy of an unscattered beam of x- or gamma- radiation per unit thickness (linear absorption coefficient), per unit mass (mass absorption coefficient), or per atom (atomic absorption coefficient) of absorber, due to transfer of energy to the absorber. -
Method of Rough Estimation of Median Lethal Dose (Ld50)
b Meta olis g m & ru D T o f x o i Journal of Drug Metabolism and l c a o n l o r Saganuwan, J Drug Metab Toxicol 2015, 6:3 g u y o J Toxicology DOI: 10.4172/2157-7609.1000180 ISSN: 2157-7609 Research Article Open Access Arithmetic-Geometric-Harmonic (AGH) Method of Rough Estimation of Median Lethal Dose (Ld50) Using Up – and – Down Procedure *Saganuwan Alhaji Saganuwan Department of Veterinary Physiology, Pharmacology and Biochemistry, College Of Veterinary Medicine, University Of Agriculture, P.M.B. 2373, Makurdi, Benue State, Nigeria *Corresponding author: Saganuwan Alhaji Saganuwan, Department of Veterinary Physiology, Pharmacology and Biochemistry, College Of Veterinary Medicine, University Of Agriculture, P.M.B. 2373, Makurdi, Benue State, Nigeria, Tel: +2348027444269; E-mail: [email protected] Received date: April 6,2015; Accepted date: April 29,2015; Published date: May 6,2015 Copyright: © 2015 Saganuwan SA . This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Earlier methods adopted for the estimation of median lethal dose (LD50) used many animals (40 – 100). But for the up – and – down procedure, 5 – 15 animals can be used, the number I still consider high. So this paper seeks to adopt arithmetic, geometric and harmonic (AGH) mean for rough estimation of median lethal dose (LD50) using up – and – down procedure by using 2 – 6 animals that may likely give 1 – 3 reversals. The administrated doses should be summed up and the mean, standard deviation (STD) and standard error of mean (SEM) should be determined. -
(LC50) of Pathogenic Microorganisms and Their Antigens in Vaccine Development Saganuwan Alhaji Saganuwan*
Saganuwan BMC Res Notes (2020) 13:289 https://doi.org/10.1186/s13104-020-05126-x BMC Research Notes RESEARCH NOTE Open Access Application of median lethal concentration (LC50) of pathogenic microorganisms and their antigens in vaccine development Saganuwan Alhaji Saganuwan* Abstract Objective: Lack of ideal mathematical models to qualify and quantify both pathogenicity, and virulence is a dreadful setback in development of new antimicrobials and vaccines against resistance pathogenic microorganisms. Hence, the modifed arithmetical formula of Reed and Muench has been integrated with other formulas and used to deter- mine bacterial colony forming unit/viral concentration, virulence and immunogenicity. Results: Microorganisms’ antigens tested are Staphylococcus aureus, Streptococcus pneumoniae, Pseudomonas aerugi- nosa in mice and rat, Edwardsiella ictaluri, Aeromonas hydrophila, Aeromonas veronii in fsh, New Castle Disease virus in chicken, Sheep Pox virus, Foot-and-Mouth Disease virus and Hepatitis A virus in vitro, respectively. The LC 50s for the pathogens using diferent routes of administrations are 1.93 103(sheep poxvirus) and 1.75 1010 for Staphylococcus × × aureus (ATCC29213) in rat, respectively. Titer index (TI) equals N log10 LC50 and provides protection against lethal dose in graded fashion which translates to protection index. N is the number of vaccine dose that could neutralize the LC50. 3 11 Hence, parasite inoculum of 10 to 10 may be used as basis for determination of LC50 and median bacterial concen- trations (BC50).Pathogenic -
Interpretation of Postmortem Toxicology Results
INTERPRETATION OF POSTMORTEM TOXICOLOGY RESULTS Pharmacogenetics and Drug-Alcohol Interaction Anna Koski Department of Forensic Medicine University of Helsinki Finland ACADEMIC DISSERTATION To be publicly discussed, with the permission of the Medical Faculty of the University of Helsinki, in the auditorium of the Department of Forensic Medicine on September 23rd 2005, at 12 noon. Helsinki 2005 SUPERVISORS Professor Antti Sajantila Department of Forensic Medicine University of Helsinki Helsinki, Finland Docent Ilkka Ojanperä Department of Forensic Medicine University of Helsinki Helsinki, Finland REVIEWERS Docent Eero Mervaala Institute of Biomedicine University of Helsinki Helsinki, Finland Docent Kari Poikolainen Finnish Foundation for Alcohol Studies National Research and Development Centre for Welfare and Health Helsinki, Finland OPPONENT Professor Jørg Mørland Division of Forensic Toxicology and Drug Abuse Norwegian Institute of Public Health Oslo, Norway ISBN 952-91-9214-2 (paperback) ISBN 952-10-2662-6 (pdf) http://ethesis.helsinki.fi Helsinki University Printing House Helsinki 2005 Obtaining a quantitative result is not the endpoint of the analytical process. Irving Sunshine CONTENTS ABBREVIATIONS......................................................................................................................... 6 LIST OF ORIGINAL PUBLICATIONS .............................................................................................. 7 ABSTRACT................................................................................................................................. -
High Degree of Acute Toxicity
Appendix I High Degree of Acute Toxicity Criteria Toxic Highly Toxic Oral LD 50 50-500 mg/kg <50 mg/kg (albino rats) Skin Contact LD 50 200-1000 mg/kg <200 mg/kg (albino rabbits, 24 hour) Inhalation LD 50 200-2000 ppm/air <200 ppm/air (albino rats, one hour) High degree of acute toxicity are chemicals that are considered highly toxic or toxic chemicals which may be fatal or cause damage to target organs as a result of a single exposure or exposures of short duration. Toxic: (a) A chemical that has a median lethal dose (LD50) of more than 50 milligrams per kilogram but not more than 500 milligrams per kilogram of body weight when administered orally to albino rats weighing between 200 and 300 grams each. (b) A chemical that has a median lethal dose (LD50) of more than 200 milligrams per kilogram but not more than 1,000 milligrams per kilogram of body weight when administered by continuous contact for 24 hours (or less if death occurs within 24 hours) with the bare skin of albino rabbits weighing between two and three kilograms each. (c) A chemical that has a median lethal concentration (LC50) in air of more than 200 parts per million but not more than 2,000 parts per million by volume of gas or vapor, or more than two milligrams per liter but not more than 20 milligrams per liter of mist, fume, or dust, when administered by continuous inhalation for one hour (or less if death occurs within one hour) to albino rats weighing between 200 and 300 grams each. -
Copper Influences the Antibacterial Outcomes of a Β-Lactamase-Activated Prochelator Against Drug-Resistant Bacteria
Article Cite This: ACS Infect. Dis. XXXX, XXX, XXX−XXX pubs.acs.org/journal/aidcbc Copper Influences the Antibacterial Outcomes of a β‑Lactamase- Activated Prochelator against Drug-Resistant Bacteria † † † ‡ Jacqueline M. Zaengle-Barone, Abigail C. Jackson, David M. Besse, Bradford Becken, ‡ § ∥ † Mehreen Arshad, Patrick C. Seed, , and Katherine J. Franz*, † Department of Chemistry, Duke University, 124 Science Drive, Durham, North Carolina 27708, United States ‡ Department of Pediatrics, Duke University, Durham, North Carolina 27710, United States § Ann and Robert H. Lurie Children’s Hospital and Stanley Manne Children’s Research Institute, 225 E. Chicago Avenue, Chicago, Illinois 60611, United States ∥ Department of Microbiology and Immunology, Northwestern University, 300 E. Superior Street, Chicago, Illinois 60611, United States *S Supporting Information ABSTRACT: The unabated rise in bacterial resistance to conventional antibiotics, coupled with collateral damage to normal flora incurred by overuse of broad-spectrum anti- biotics, necessitates the development of new antimicrobials targeted against pathogenic organisms. Here, we explore the antibacterial outcomes and mode of action of a prochelator that exploits the production of β-lactamase enzymes by drug- resistant bacteria to convert a nontoxic compound into a metal-binding antimicrobial agent directly within the microenvironment of pathogenic organisms. Compound PcephPT (phenylacetamido-cephem-pyrithione) contains a cephalosporin core linked to 2-mercaptopyridine N-oxide (pyrithione) via one of its metal-chelating atoms, which minimizes its preactivation interaction with metal ions and its cytotoxicity. Spectroscopic and chromatographic assays indicate that PcephPT releases pyrithione in the presence of β-lactamase-producing bacteria. The prochelator shows enhanced antibacterial activity against strains expressing β-lactamases, with bactericidal efficacy improved by the presence of low-micromolar copper in the growth medium. -
Median Lethal Dose (LD50) Estimation of Β-Cyfluthrin in Male and Female Swiss Albino Mice
International Journal of Scientific and Research Publications, Volume 5, Issue 8, August 2015 1 ISSN 2250-3153 Median lethal dose (LD50) estimation of β-cyfluthrin in male and female Swiss albino mice # # Neelu Kanwar Rajawat , Rajbala Verma , Inderpal Soni Environmental Toxicology Lab, Centre for Advanced Studies, Department of Zoology, University of Rajasthan, Jaipur 302004 India # Equal contribution Abstract- Present study was undertaken to determine the median documented in rats but satisfactory data related to LD50 in mice lethal dose (LD50) of β-cyfluthrin (β-cyf), a synthetic (type II) is not available. Moreover there is a difference in LD50 of β-cyf pyrethroid pesticide in male and female Swiss albino mice. The in male and female animals and also with different vehicles. Thus calculation of LD 50 is an initial screening step in the assessment an attempt was made to determine the acute oral LD50 of β-cyf in and evaluation of the toxic characteristic of a chemical substance. male and female Swiss albino mice using corn oil as vehicle. The selected single doses of β-cyfluthrin based on the pilot study were 200, 225, 250, 275 and 300 mg/kg b.wt. for male and 350, 375, 400, 425 and 450 mg/kg b.wt. for female animals. Pesticide II. MATERIALS AND METHODS was dissolved in corn oil and administered orally to different groups of male and female mice, consisting of 10 animals in each group. Signs of toxicity and possible death of animals were Test chemicals β-cyf (CAS No. 68359-37-5) was purchased from Sigma- monitored upto 96 h to calculate the median lethal dose (LD50) of β-cyf. -
The Calculation of Median Lethal Dose (LD50) and Maximum Permissible Dose (MPD) Values of Sodium Arsenite in Female Swiss Albino Mice
IOSR Journal of Environmental Science, Toxicology and Food Technology (IOSR-JESTFT) e-ISSN: 2319-2402,p- ISSN: 2319-2399.Volume 12, Issue 9 Ver. I (September. 2018), PP 89-91 www.iosrjournals.org The Calculation of Median Lethal Dose (LD50) And Maximum Permissible Dose (MPD) Values of Sodium Arsenite In Female Swiss Albino Mice *Shailendra Kumar And Preety Sinha Departement of Zoology, A. N. College, Patna, Bihar, India. Corresponding Author: Shailendra Kumar Abstract: Sodium arsenite is an environmental pollutant and is responsible for both knowing poisonings and accidental exposures that can cause harmful health issues and possibly death. Median lethal dose (LD50) is a statistically obtained dose of a compound that can be predicted to cause death in 50% of the mice when administered by a specific route as a single dose and mice noticed for a specific time period. In the present research, different doses i.e., 6, 9, 12, 15, 18, 21 and 24 mg/kg body weight of Sodium arsenite was given orally by gavage method to the seven different groups of Swiss albino mice. Signs and symptoms of toxicity and probable death of mice were observed for 3 hours and then at 6, 12, 24, 48 and 72 hours to calculate the Median lethal dose (LD50) and maximum permissible dose (MPD) of Sodium arsenite. The LD50 was found to 18 mg/kg body weight after oral administration in Swiss albino mice. Finally, MPD of Sodium arsenite by oral route in mice was found to be 1.8 mg/kg body weight. Keywords: Sodium arsenite, Swiss albino mice, LD50, MPD ----------------------------------------------------------------------------------------------------------------------------- ---------- Date of Submission: 27-08-2018 Date of acceptance: 11-09-2018 ----------------------------------------------------------------------------------------------------------------------------- ---------- I. -
Gate Frame Question
UNIT THREE BIOLOGICAL EFFECTS AND INTERNAL HAZARDS OF RADIATION EXPOSURE Unit Two reviewed the mechanism by which ionizing radiation may cause biological damage. That mechanism can be summarized by saying that ions created by radiation, as well as new compounds formed by the pairing up of the ions, disrupt cell organization and function. For radiological emergency responders, the potential biological effects of radiation exposure are important considerations. You have studied biological effects and internal hazards of radiation in other courses. This unit will incorporate a review of some important basic concepts and introduce a few new terms and details that will better prepare you for radiological emergency response operations. GATE FRAME You have responded to an accident involving a truck containing radionuclides destined for a research facility. QUESTION The Incident Commander tells you that a package found on the ground indicates that it contains 0.2 Ci of iodine-131 (I-131). I-131 is a beta emitter, with a radioactive half-life of 8 days. What potential biological effects are associated with radia- tion exposure to this type of material, and what factors determine the extent of potential biological damage by this material? (Use another sheet if needed.) 3-1 Unit Three Biological Effects and Internal Hazards of Radiation Exposure ANSWER The radiation health effects from beta-emitting radionuclides such as I-131 may be early (acute) or late (chronic). Early affects, which occur within two or three months after exposure, include skin damage (such as “beta burns”), loss Your answer should of appetite, nausea, fatigue, and diarrhea. Late effects, include the adjacent which can occur years after exposure, include cancer, information. -
Open Natural Products Research: Curation and Dissemination of Biological Occurrences of Chemical Structures Through Wikidata
bioRxiv preprint doi: https://doi.org/10.1101/2021.02.28.433265; this version posted March 1, 2021. The copyright holder has placed this preprint (which was not certified by peer review) in the Public Domain. It is no longer restricted by copyright. Anyone can legally share, reuse, remix, or adapt this material for any purpose without crediting the original authors. Open Natural Products Research: Curation and Dissemination of Biological Occurrences of Chemical Structures through Wikidata Adriano Rutz1,2, Maria Sorokina3, Jakub Galgonek4, Daniel Mietchen5, Egon Willighagen6, James Graham7, Ralf Stephan8, Roderic Page9, Jiˇr´ıVondr´aˇsek4, Christoph Steinbeck3, Guido F. Pauli7, Jean-Luc Wolfender1,2, Jonathan Bisson7, and Pierre-Marie Allard1,2 1School of Pharmaceutical Sciences, University of Geneva, CMU - Rue Michel-Servet 1, CH-1211 Geneva 4, Switzerland 2Institute of Pharmaceutical Sciences of Western Switzerland, University of Geneva, CMU - Rue Michel-Servet 1, CH-1211 Geneva 4, Switzerland 3Institute for Inorganic and Analytical Chemistry, Friedrich-Schiller-University Jena, Lessingstr. 8, 07732 Jena, Germany 4Institute of Organic Chemistry and Biochemistry of the CAS, Flemingovo n´amˇest´ı2, 166 10, Prague 6, Czech Republic 5School of Data Science, University of Virginia, Dell 1 Building, Charlottesville, Virginia 22904, United States 6Dept of Bioinformatics-BiGCaT, NUTRIM, Maastricht University, Universiteitssingel 50, NL-6229 ER, Maastricht, The Netherlands 7Center for Natural Product Technologies, Program for Collaborative Research -
Dose - Response Relationships • Interpret Frequency (Normal Distribution) and Dose - Response Curves
Principles of Environmental Toxicology Learning Objectives • Understand the quantitative relationship between toxicant exposure and induced effects. • Describe frequently encountered toxic effects. Dose - Response Relationships • Interpret frequency (normal distribution) and dose - response curves. • Understand threshold Principles of Environmental Toxicology effects with dosage Instructor: Gregory Möller, Ph.D. increase. University of Idaho 2 Principles of Environmental Toxicology Principles of Environmental Toxicology Learning Objectives, 2 What is a Dose? • Understand effective dose, margin-of-safety and • The amount of a substance administered at the relationship of effective vs. toxic dose. one time. • Examine the use of actual data for no observed • Dosage is the amount per unit weight of the effect and lowest observed exposed individual. effect in risk assessments. • Exposure is characterized • Summarize effective, lethal by and toxic doses. – Number of doses • Understand a linearized – Frequency of dosing multi-stage model for – The total period of time non-threshold responses. for the exposure. 3 4 Principles of Environmental Toxicology Principles of Environmental Toxicology Quantifying the Dose Key Concepts • Gram (g) is the standard unit but mg is typical • Dosage - response mathematical relationship of most exposures in toxicology. (positive slope). • Dosage: mg (dose) / kg (bw) / day (duration) • Causal relationship. –mg/kg/d • Observable responses. • Exposures are quantified in relation to the • Statistical management of variability media. of individual responses. – mg/L in water. – mg/kg in food. – Species, genetics, age, sex. –mg/m3 in air. • Variation in units common (ppm, ppb). 5 6 1 Principles of Environmental Toxicology Principles of Environmental Toxicology Responses (Toxic Effects) Responses (Toxic Effects), 2 • Inflammation. • Lethal synthesis. – Local or systemic response.