TOPIC 5 Lab – B: Diagnostic Tools & Therapies – Blood & Lymphatic
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The Developmental Genetics of Hemoglobin Synthesis in Chironomus Darrel Starr English Iowa State University
Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 1968 The developmental genetics of hemoglobin synthesis in Chironomus Darrel Starr English Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Genetics Commons Recommended Citation English, Darrel Starr, "The developmental genetics of hemoglobin synthesis in Chironomus " (1968). Retrospective Theses and Dissertations. 3660. https://lib.dr.iastate.edu/rtd/3660 This Dissertation is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. This dissertation has been microfilmed exactly as received 6 8-14,785 ENGLISH, Barrel Starr, 1936- THE DEVELOPMENTAL GENETICS OF HEMOGLOBIN SYNTHESIS IN CHIRONOMUS. Iowa State University, Ph.D., 1968 Biology- Genetics University Microfilms, Inc., Ann Arbor, Michigan THE DEVELOPMENTAL GENETICS OF HEMOGLOBIN SYNTHESIS IN CHIRONOMUS by Darrel Starr English A Dissertation Submitted to the Graduate Faculty in Partial Fulfillment of The Requirements for the Degree of DOCTOR OF PHILOSOPHY Major Subject: Genetics Approved: Signature was redacted for privacy. In Charge of MajdA Work Signature was redacted for privacy. Head ^ Major Department Signature was redacted for privacy. -
University of Illinois College of Medicine at Urbana-Champaign
UNIVERSITY OF ILLINOIS COLLEGE OF MEDICINE AT URBANA-CHAMPAIGN PATHOLOGY - VOLUME I 2014 - 2015 PATHOLOGY TEACHING FACULTY LIST Jerome Anderson, MD Farah Gaudier, MD Richard Tapping, PhD Department of Pathology Dept. of Pathology Associate Professor. McDonough District Hosp. Carle Physician Group Dept. of Microbiology McComb, IL 61455 [email protected] [email protected] Phone: (309) 837-2368 [email protected] Teaching Assistant Nasser Gayed, MD Lindsey Burnett, PhD Brett Bartlett, MD Dept. of Med. Info. Sciences [email protected] Dept. of Pathology 190 Medical Sciences Bldg SBL Health Centre 506 South Mathews Avenue Mattoon, IL 61938 Urbana, IL 61801 Pathology Office [email protected] [email protected] Jackie Newman Phone: (217) 244-2265 Frank Bellafiore, MD Nicole Howell, MD [email protected] Dept. of Pathology Dept. of Pathology Carle Physician Group Carle Physician Group 602 West University Avenue [email protected] Urbana, IL 61801 [email protected] Zheng George Liu, MD Dept. of Pathology Allan Campbell, MD Carle Physician Group Dept. Of Pathology 602 West University Avenue UICOM Peoria IL Urbana, IL 61801 [email protected] [email protected] Gregory Freund, MD Steve Nandkumar, M.D. Head, Dept. of Pathology Pathology Course Director 190 Medical Sciences Building 249 Medical Sciences Building 506 South Mathews Avenue 506 South Mathews Avenue Urbana, IL 61801 Urbana, IL 61801 [email protected] [email protected] Page 2 Pathology M-2 Introduction INTRODUCTION Pathology – study of the essential nature of diseases and the structural and functional changes produced by them. ( Pathos= suffering; ologos = study) Pathology consists of two major subdivisions. -
Modelling of Red Blood Cell Morphological and Deformability Changes During In-Vitro Storage
applied sciences Article Modelling of Red Blood Cell Morphological and Deformability Changes during In-Vitro Storage Nadeeshani Geekiyanage 1 , Emilie Sauret 1,*, Suvash Saha 2 , Robert Flower 3 and YuanTong Gu 1 1 School of Mechanical, Medical and Process Engineering, Science and Engineering Faculty, Queensland University of Technology (QUT), Brisbane City, QLD 4000, Australia; [email protected] (N.G.); [email protected] (Y.G.) 2 School of Mechanical and Mechatronic Engineering, University of Technology Sydney (UTS), Ultimo, NSW 2007, Australia; [email protected] 3 Research and Development, Australian Red Cross Lifeblood, Kelvin Grove, QLD 4059, Australia; [email protected] * Correspondence: [email protected] Received: 28 February 2020; Accepted: 27 April 2020; Published: 4 May 2020 Featured Application: Red blood cell (RBC) storage lesion is a critical issue facing transfusion treatments, and significant changes in RBC morphology and deformability are observed due to the storage lesion. RBCs require high deformability to sustain in-vivo circulation, and impaired deformability leads to several post-transfusion adverse outcomes. Therefore, improved understanding of the interrelation between the morphological and deformability changes and the quality and viability of the stored RBCs is essential to prevent or reduce the transfusion related adverse outcomes. To support this requisite, the influence on RBC deformability due to several aspects of the storage lesion, namely, the changes in cell morphology, surface area and volume, RBC membrane biomechanics, and cytoskeletal structural integrity are explored numerically in this study. Abstract: Storage lesion is a critical issue facing transfusion treatments, and it adversely affects the quality and viability of stored red blood cells (RBCs). -
8.5 X12.5 Doublelines.P65
Cambridge University Press 978-0-521-87519-6 - Disorders of Hemoglobin: Genetics, Pathophysiology, and Clinical Management, Second Edition Edited by Martin H. Steinberg, Bernard G. Forget, Douglas R. Higgs and David J. Weatherall Index More information anti-inflammatory therapy, 762–763 thalassemia-related complications, 779 sulfasalazine, nuclear factor (NF)-kB, 762 transplant-related complications, 778–779 targeting ET-1, 762–763 S-linked haplotypes, African/Indo-European, anti-oxidant therapy targeting erythrocyte, 638–640 765–766 burst forming unit-erythroid (BFU-E), 10, 29 deferiprone, 765 oral glutamine, 765 calcium-activated potassium channel (Gardos oral N-acetyl-cysteine, 765–766 pathway), 167–168 anti-oxidant therapy targeting vascular, 763–765 capillary electrophoresis, 660 Index Apo A-I mimetics, 764 capillary IEF, 660 NO, 763–764 carbon monoxide poisoning, 613–616 statins, 764 clinical features, 615 xanthine oxidase inhibitors, 764–765 diagnosis, treatment, 615–616 anti-thrombotic therapy epidemiology, 613–614 -thalassemia, 761–762 cardiac, arterial abnormalities, 151 sickle cell disease, 761–762 cardiac abnormalities, ATRX syndrome, 305 aortagonad-mesonephros (AGM), 6 cardiovascular disease, 652 Apo A-I mimetics, 764 cation content, cellular hydration, 164–172 apoptosis, vasculature permeability, 193–194 calcium-activated potassium channel, 167–168 assays, assay systems, 7, 142 cation permeability alterations, 166–167 ATMDS. See ␣ thalassemia-myelodysplastic cell calcium, calcium pump activity, 167 syndromes cell sodium, -
Erythrocytes: Overview, Morphology, Quantity by AH Rebar Et
In: A Guide to Hematology in Dogs and Cats, Rebar A.H., MacWilliams P.S., Feldman B.F., Metzger F.L., Pollock R.V.H. and Roche J. (Eds.). Publisher: Teton NewMedia, Jackson WY (www.veterinarywire.com). Internet Publisher: International Veterinary Information Service, Ithaca NY (www.ivis.org), 8-Feb-2005; A3304.0205 Erythrocytes: Overview, Morphology, Quantity A.H. Rebar1, P.S. MacWilliams2, B.F. Feldman 3, F.L. Metzger 4, R.V.H. Pollock 5 and J. Roche 6 1Dept of Veterinary Pathobiology, School of Veterinary Medicine, Purdue University, IN,USA. 2Dept of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, WI, USA. 3Dept of Biomedical Sciences & Pathobiology, VA-MD - Regional College of Veterinary Medicine, Virginia Tech, VA, USA. 4Metzger Animal Hospital,State College,PA, USA. 5Fort Hill Company, Montchanin, DE, USA. 6 Hematology Systems, IDEXX Laboratories, Westbrook, ME, USA. Overview Production Red blood cells (RBC) are produced in the bone marrow. Numbers of circulating RBCs are affected by changes in plasma volume, rate of RBC destruction or loss, splenic contraction, erythropoietin (EPO) secretion, and the rate of bone marrow production. A normal PCV is maintained by an endocrine loop that involves generation and release of erythropoietin (EPO) from the kidney in response to renal hypoxia. Erythropoietin stimulates platelet production as well as red cell production. However, erythropoietin does not stimulate white blood cell (WBC) production. Erythropoiesis and RBC numbers are also affected by hormones from the adrenal cortex, thyroid, ovary, testis, and anterior pituitary. Destruction Red cells have a finite circulating lifespan. In dogs, the average normal red cell circulates approximately 100 days. -
Newborn Screening Result for Bart's Hemoglobin
NEWBORN SCREENING RESULT FOR BART’S HEMOGLOBIN Physician’s information sheet developed by the Nebraska Newborn Screening Program with review by James Harper, MD, Pediatric Hematologist with UNMC Follow-up program, and member of the Nebraska Newborn Screening Advisory Committee. BACKGROUND The alpha thalassemias result from the loss of alpha globin genes. There are normally four genes for alpha globin production so that the loss of one to four genes is possible. The lack of one gene causes alpha thalassemia 2 (silent carrier) with no clinically detectable problems but may cause small amounts of hemoglobin Barts to be present in newborn blood samples. Alpha thalassemia trait (Alpha thalassemia 1) results from loss of two genes and causes a mild microcytic anemia which may resemble iron deficiency anemia. The loss of three genes causes hemoglobin H diseases which is a moderately severe form of thalassemia. The lack of all four genes causes hydrops fetalis and is usually fatal in utero. In general, only the loss of one or two genes is seen in African Americans. Individuals from Southeast Asia and the Mediterranean may have all four types of alpha thalassemia. The percentage of hemoglobin Barts in the blood sample may indicate the number of alpha genes that have been lost. However, the percentage of hemoglobin Barts is not directly measurable with the current methodology used by the newborn screening laboratory. Only the presence of Barts hemoglobin in relation to fetal and adult hemoglobin, and variants S, C, D and E can be detected. RECOMMENDED WORK UP In addition to the standard newborn hemoglobinopathy confirmation (hemoglobin electrophoresis), to separate those patients with alpha thalassemia silent carrier from the patients with alpha thalassemia trait, we recommend that these babies have the following labs drawn at their 6 month well baby check: CBC with retic count, ferritin, and a hemoglobin electropheresis. -
Thrombotic Microangiopathy Score As a New Predictor for Neurologic Outcome in Patients Undergoing Targeted Temperature Management After Out-Of-Hospital Cardiac Arrest
Thrombotic Microangiopathy Score as a New Predictor for Neurologic Outcome in Patients Undergoing Targeted Temperature Management After Out-of-hospital Cardiac Arrest Taeyoung Kong Yonsei University College of Medicine Hye Sun Lee Yonsei University College of Medicine Soyoung Jeon Yonsei University College of Medicine Jong Wook Lee Konyang University Hospital Hyun Soo Chung Yonsei University College of Medicine Sung Phil Chung Yonsei University College of Medicine Je Sung You ( [email protected] ) Yonsei University College of MedicineGangnam Severance Hospital https://orcid.org/0000-0002-2074- 6745 Original research Keywords: Out-of-hospital cardiac arrest, Targeted temperature management, Thrombotic microangiopathy score, Mortality, Predictor, Schistocytes Posted Date: July 8th, 2020 DOI: https://doi.org/10.21203/rs.3.rs-40096/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/21 Abstract Background: Given the morphological characteristics of schistocytes, thrombotic microangiopathy (TMA) score can be benecial as it can be quickly and serially measured without additional effort or costs. This study aimed to investigate whether the serial TMA scores until 48 h post admission are associated with clinical outcomes in patients undergoing targeted temperature management (TTM) after out-of-hospital cardiac arrest (OHCA). Methods:We retrospectively evaluated a cohort of 185 patients using a prospective registry. We analyzed the TMA score at admission and after 12, 24, and -
LOINC Top 2000++ Lab Observations V1.6 (PDF)
LOINC Mapper's Guide to Top 2000++ US Lab Tests v1.6 June 2017 Page 1 of 112 B C EFGH I P LOINC # Long Common Name Class Rank Example Example Comments System Override UCUM UCUM Adjusted 1 Display 2 General Guidance 1) Ask your test kit and instrument manufacturer(s) and referral labs about which LOINC codes are relevant for their products. Increasingly, test kit and instrument manufacturers are requesting LOINC codes for their new test. Some of the larger manufacturers have mapped their routine tests done on to LOINC codes. Check with these in vitro diagnostic companies for the LOINC codes relevant for their tests. In addition, the largest referral laboratories in the US have mapped their high- to medium-volume tests to LOINC. Getting the LOINC mappings from either of these sources will save you time. 2) When mapping, search against the LOINC common test list. In RELMA and on search.loinc.org you can set the search parameters to only look at the common tests. Work through the mapping by lab section. Realize that LOINC does not encompass terms that may be used in your lab system for internal accounting or “diagnostic” variables that are provided as indicators that might be used to trigger a follow up test, but are not supposed to be reported to the ordering provider because the results are not reliable enough. Blood cell counters usually report such indicators. 3) Obtain a master list of tests for mapping. RELMA has a function that will convert a large set of HL7 result (ORU) messages into a database that carries the name of the order, the units of measure, and sample data that can be the source of frequency statistics for deciding which terms to tackle first. -
Rbcs) in Both the Sinus and Cord, Histiocytes Werc Swollen by a Granu}Ar Substance in the Cytoplasm and Also Many Secondary Lysosomes
The UOEHAssociationUOEH Association ofofHealth Health Sciences JUOEH20(1)!11-19 (1998) 11 [Original) Pathological Study Splenomegaly Associated with Cadmium-inducedof Anemia in Rats Tetsuo HAMADA', Akihide TANIMOT02, Nobuyuki ARIMA!, Yoshihiro IDEL, Takakazu SASAGURI2, Shohei SHIMiVIRI2, Yoshitaka MURATA', Ke-Yong WANG2 and Yasuyuki SASAGURIL' 'Dopartment of'Surgical Pathotogy, University llosPital ?Dopartment qf Palhology and Cell Biotogy, Scheol of' Adlrdicine, (1itib'ersity of Occapational and Environmental Health., .lapan. }'dhatanishi-ku, Kiialp,ztshu 807-8imr, .1apan Ahstract : Splenomegaly was observcd both in male and R)malc Spraguc-Dawley rats after 1 week of exposure to CdC12 (O,6 mg (:d/kg/day), Sp]een weight reached about double that in controls by 8 weeks of Cd exposure. Histopathologica] cxamination of the enlargcd spleen rcvcaled that iron- and lipid-laden histiocytes were clustered in tha periarterial lymphatic sheath, and the red pulp appeared to be expanded. It is noteworthy that electron microscopy rcvealed markcd poikilocytosis and Hcinz body formation in red blood cells (RBCs) in both the sinus and cord, Histiocytes werc swollen by a granu}ar substance in the cytoplasm and also many secondary lysosomes. Thesc morphological findings indicatc that degradation of damagcd RBCs induced by exposure to Cd might bc promoted in the splccn and possibly cause splenomcgaly, This RBC damage-hcmolysis-splcnomegaly sequence is also considered to be associated with the etioiogy of Cd-induced anemia, In addition to the abnormal RBC degradation, nuclel of ]ymphocytes in thc Cd-cxposcd spleen exhibited high elcctron density, consistent with a preapoptotic statc suggesting the immunosupprcssive effhct ofCd. Kay woralf :spienomegaly, poiki]ocytosis, Heinz body, cadmiurn, anemia, (Received 18 November 1997, accepted I9January 1998) Introduction Cd was reported to cause anemia in dogs as early as 1896 [1], and subsequently, anemia was found in humans after Cd exposure [2]. -
Code Lists Page 1
Code lists Page 1 Code lists AESEV Page 2 AESEV Codelist Name: Severity/Intensity Scale for Adverse Events Description: A scale that defines the degree or state of disease existing in a patient as a result of the occurrence of an adverse event. (NCI) C41338,1; Grade 1 C41339,2; Grade 2 C41340,3; Grade 3 AGEU Page 3 AGEU Codelist Name: Age Unit Description: Those units of time that are routinely used to express the age of a subject. C25301,Days C25529,Hours; h; hr C29846,Month C29844,Week C29848,Year CMDOSFRM Page 4 CMDOSFRM Codelist Name: Concomitant Medication Dose Form Description: A terminology subset of the CDISC SDTM Pharmaceutical Dosage Form codelist created for CDASH Concomitant Medication Dose Form codelist. (NCI) C42887,AEROSOL; aer C25158,CAPSULE; cap C28944,CREAM; C42933,GAS; C42934,GEL; C42966,OINTMENT; oint C42968,PATCH; C42972,POWDER; C42989,SPRAY; C42993,SUPPOSITORY; supp C42994,SUSPENSION; susp C42998,TABLET; tab CMDOSFRQ Page 5 CMDOSFRQ Codelist Name: Concomitant Medication Dosing Frequency per Interval Description: A terminology subset of the CDISC SDTM Frequency codelist created for CDASH Concomitant Medication Dosing Frequency per Interval codelist. (NCI) C64496,BID; BD; Twice per day C64499,PRN; As needed C25473,QD; Daily C64530,QID; 4 times per day C64498,QM; Every Month; Per Month C64525,QOD; Every other day C64527,TID; 3 times per day C17998,UNKNOWN; U; UNK; Unknown CMDOSU Page 6 CMDOSU Codelist Name: Concomitant Medication Dose Units Description: A terminology subset of the CDISC SDTM Unit codelist created for CDASH Concomitant Medication Dose Units codelist. (NCI) C48480,CAPSULE; Capsule Dosing Unit; cap C48155,g; Gram C48579,IU; IE; International Unit C28253,mg; Milligram C28254,mL; Milliliter; cm3 C65060,PUFF; Puff Dosing Unit C48542,TABLET; Tablet Dosing Unit; tab C48152,ug; Microgram; mcg CMROUTE Page 7 CMROUTE Codelist Name: Concomitant Medication Route of Administration Description: A terminology subset of the CDISC SDTM Route codelist created for CDASH Concomitant Medication Route of Administration codelist. -
Morphological Study of Human Blood for Different Diseases
Research Article ISSN: 2574 -1241 DOI: 10.26717/BJSTR.2020.30.004893 Morphological Study of Human Blood for Different Diseases Muzafar Shah1*, Haseena1, Kainat1, Noor Shaba1, Sania1, Sadia1, Akhtar Rasool2, Fazal Akbar2 and Muhammad Israr3 1Centre for Animal Sciences & Fisheries, University of Swat, Pakistan 2Centre for Biotechnology and Microbiology, University of Swat, Pakistan 3Department of Forensic Sciences, University of Swat, Pakistan *Corresponding author: Muzafar Shah, Centre for Animal Sciences & Fisheries, University of Swat, Pakistan ARTICLE INFO ABSTRACT Received: August 25, 2020 The aim of our study was the screening of blood cells on the basis of morphology for different diseased with Morphogenetic characters I e. ear lobe attachment, clinodactyly Published: September 07, 2020 and tongue rolling. For this purpose, 318 blood samples were collected randomly. Samples were examined under the compound microscopic by using 100x with standard Citation: Muzafar Shah, Haseena, method. The results show 63 samples were found normal while in 255 samples, different Kainat, Noor Shaba, Sania, Sadia, et al. types of morphological changes were observed which was 68.5%, in which Bite cell 36%, Morphological Study of Human Blood for Elliptocyte 34%, Tear drop cell 30%, Schistocyte 26%, Hypochromic cell 22.5%, Irregular Different Diseases. Biomed J Sci & Tech Res contracted cell 16%, Echinocytes 15.5%, Roleaux 8%, Boat shape 6.5%, Sickle cell 5%, Keratocyte 4% and Acanthocytes 1.5%. During the screening of slides, bite cell, elliptocyte, tear drop cell, schistocytes, hypochromic cell, irregular contracted cells were found 30(1)-2020.Keywords: BJSTR.Human MS.ID.004893. blood; Diseases; frequently while echinocytes, boat shape cell, acanthocytes, sickle cells and keratocytes Morphological; Acanthocytes; Keratocyte were found rarely. -
Complete Blood Count in Primary Care
Complete Blood Count in Primary Care bpac nz better medicine Editorial Team bpacnz Tony Fraser 10 George Street Professor Murray Tilyard PO Box 6032, Dunedin Clinical Advisory Group phone 03 477 5418 Dr Dave Colquhoun Michele Cray free fax 0800 bpac nz Dr Rosemary Ikram www.bpac.org.nz Dr Peter Jensen Dr Cam Kyle Dr Chris Leathart Dr Lynn McBain Associate Professor Jim Reid Dr David Reith Professor Murray Tilyard Programme Development Team Noni Allison Rachael Clarke Rebecca Didham Terry Ehau Peter Ellison Dr Malcolm Kendall-Smith Dr Anne Marie Tangney Dr Trevor Walker Dr Sharyn Willis Dave Woods Report Development Team Justine Broadley Todd Gillies Lana Johnson Web Gordon Smith Design Michael Crawford Management and Administration Kaye Baldwin Tony Fraser Kyla Letman Professor Murray Tilyard Distribution Zane Lindon Lyn Thomlinson Colleen Witchall All information is intended for use by competent health care professionals and should be utilised in conjunction with © May 2008 pertinent clinical data. Contents Key points/purpose 2 Introduction 2 Background ▪ Haematopoiesis - Cell development 3 ▪ Limitations of reference ranges for the CBC 4 ▪ Borderline abnormal results must be interpreted in clinical context 4 ▪ History and clinical examination 4 White Cells ▪ Neutrophils 5 ▪ Lymphocytes 9 ▪ Monocytes 11 ▪ Basophils 12 ▪ Eosinophils 12 ▪ Platelets 13 Haemoglobin and red cell indices ▪ Low haemoglobin 15 ▪ Microcytic anaemia 15 ▪ Normocytic anaemia 16 ▪ Macrocytic anaemia 17 ▪ High haemoglobin 17 ▪ Other red cell indices 18 Summary Table 19 Glossary 20 This resource is a consensus document, developed with haematology and general practice input. We would like to thank: Dr Liam Fernyhough, Haematologist, Canterbury Health Laboratories Dr Chris Leathart, GP, Christchurch Dr Edward Theakston, Haematologist, Diagnostic Medlab Ltd We would like to acknowledge their advice, expertise and valuable feedback on this document.