View Table of Contents

Total Page:16

File Type:pdf, Size:1020Kb

View Table of Contents Table of Contents Preface. xv About the Authors . xvii Section 1: ABO: The Birth of Blood Groups 1. Blood Groups—From Then ’Til Now . .1 Discovery . .1 Response and Reconsideration . .2 Beyond ABO . .4 M, N, and P . .5 Rh . .6 The Antiglobulin Test . .7 The Plot Thickens . .7 References . .8 2. Karl Landsteiner, Father of Blood Groups . .9 Beginnings . .9 Medical School . .11 The Young Researcher . .13 Priority Issues . .16 Decastello and Sturli: Another Blood Group . .18 Other Directions . .19 Life in Vienna . .21 References . .23 3. ABO Grows Up . .27 Transfusion History, 1600 to 1920 . .27 The Blood Groups Gain Attention . .29 Transfusion in World War I . .37 Advances in ABO Blood Group Serology . .39 References . .47 4. Genetics, Eugenics, and Blood Groups . .51 Heredity, 1900 . .52 The Rise of Genetics . .52 Genes and Blood Groups . .53 viii BLOODY BRILLIANT! Genes and Populations . 59 References . 62 5. Karl Landsteiner in New York . 65 At “The Rockefeller” . 65 Landsteiner Returns to the Blood Groups . 68 The Nobel Prize . 71 The Laureate at Work . 73 References . 74 6. Out, Damned Spot! Early Forensic Applications of ABO . 77 What Blood Can Tell . 78 Is It Blood? . 78 Is It Human Blood? . 79 Whose Blood Is It? . 81 References . 85 7. Who’s Your Daddy? ABO and Paternity Testing . 87 Establishing Paternity . 87 Paternity Testing and the Courts: Europe . 89 Paternity Testing and the Courts: Britain . 91 Paternity Testing and the Courts: United States . 92 Lights! Camera! Action! . ..
Recommended publications
  • Requirements for Blood and Blood Components Intended for Transfusion Or for Further Manufacturing Use
    Requirements for Blood and Blood Components Intended for Transfusion or for Further Manufacturing Use Office of Blood Research and Review CBER, FDA Ask the FDA Session – AABB Annual Meeting October 26, 2015 1 Outline • Overview – Historical Background – Intent of the Rule – Organization of the Rule • Selected Provisions – Relevant Transfusion-Transmitted Infection – Control of Bacterial Contamination of Platelets – Medical Supervision – Donor Acknowledgement – Alternative Procedures – Donor Eligibility • Implementation 2 GAO Oversight and FDA Concerns • Publish in the form of regulations the guidelines that FDA deems essential to ensure the safety of the blood supply • Concern about the delay in requiring testing for emerging infectious agents, e.g. HTLV • Concern about blood safety and the regulations being out-of-date • Concerns about donor safety 3 Intent of the Final Rule • To better assure the safety of the blood supply and to help protect donor health • To make donor eligibility and testing requirements more consistent with current practices and to provide flexibility with regard to emerging infectious diseases • To accommodate technological advances • To establish requirements for donor education, donor history, and donor testing 4 Organization of the Final Rule - 1 • A. General • B. Definitions (§§ 606.3, 610.39, 630.3, 640.125) • C. Standard Operating Procedures (§ 606.100) • D. Control of Bacterial Contamination of Platelets (§ 606.145) • E. Records (§ 606.160) • F. Test Requirements (§§ 610.40, 640.5, 640.71(a)) • G. Donor Deferral (§ 610.41) 5 Organization of the Final Rule - 2 • H. Purpose and Scope (§ 630.1) • I. Medical Supervision (§ 630.5) • J. General Donor Eligibility Requirements(§ 630.10) • K. Donor Eligibility Requirements Specific to Whole Blood, Red Blood Cells and Plasma Collected by Apheresis (§ 630.15) • L.
    [Show full text]
  • 27. Clinical Indications for Cryoprecipitate And
    27. CLINICAL INDICATIONS FOR CRYOPRECIPITATE AND FIBRINOGEN CONCENTRATE Cryoprecipitate is indicated in the treatment of fibrinogen deficiency or dysfibrinogenaemia.1 Fibrinogen concentrate is licenced for the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenaemia and hypofibrinogenaemia,2 and is currently funded under the National Blood Agreement. Key messages y Fibrinogen is an essential component of the coagulation system, due to its role in initial platelet aggregation and formation of a stable fibrin clot.3 y The decision to transfuse cryoprecipitate or fibrinogen concentrate to an individual patient should take into account the relative risks and benefits.3 y The routine use of cryoprecipitate or fibrinogen concentrate is not advised in medical or critically ill patients.2,4 y Cryoprecipitate or fibrinogen concentrate may be indicated in critical bleeding if fibrinogen levels are not maintained using FFP. In the setting of major obstetric haemorrhage, early administration of cryoprecipitate or fibrinogen concentrate may be necessary.3 Clinical implications y The routine use of cryoprecipitate or fibrinogen concentrate in medical or critically ill patients with coagulopathy is not advised. The underlying causes of coagulopathy should be identified; where transfusion is considered necessary, the risks and benefits should be considered for each patient. Specialist opinion is advised for the management of disseminated intravascular coagulopathy (MED-PP18, CC-PP7).2,4 y Cryoprecipitate or fibrinogen concentrate may be indicated in critical bleeding if fibrinogen levels are not maintained using FFP. In patients with critical bleeding requiring massive transfusion, suggested doses of blood components is 3-4g (CBMT-PP10)3 in adults or as per the local Massive Transfusion Protocol.
    [Show full text]
  • Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse
    Welcome to More Choice CD Marker Handbook For more information, please visit: Human bdbiosciences.com/eu/go/humancdmarkers Mouse bdbiosciences.com/eu/go/mousecdmarkers Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse CD3 CD3 CD (cluster of differentiation) molecules are cell surface markers T Cell CD4 CD4 useful for the identification and characterization of leukocytes. The CD CD8 CD8 nomenclature was developed and is maintained through the HLDA (Human Leukocyte Differentiation Antigens) workshop started in 1982. CD45R/B220 CD19 CD19 The goal is to provide standardization of monoclonal antibodies to B Cell CD20 CD22 (B cell activation marker) human antigens across laboratories. To characterize or “workshop” the antibodies, multiple laboratories carry out blind analyses of antibodies. These results independently validate antibody specificity. CD11c CD11c Dendritic Cell CD123 CD123 While the CD nomenclature has been developed for use with human antigens, it is applied to corresponding mouse antigens as well as antigens from other species. However, the mouse and other species NK Cell CD56 CD335 (NKp46) antibodies are not tested by HLDA. Human CD markers were reviewed by the HLDA. New CD markers Stem Cell/ CD34 CD34 were established at the HLDA9 meeting held in Barcelona in 2010. For Precursor hematopoetic stem cell only hematopoetic stem cell only additional information and CD markers please visit www.hcdm.org. Macrophage/ CD14 CD11b/ Mac-1 Monocyte CD33 Ly-71 (F4/80) CD66b Granulocyte CD66b Gr-1/Ly6G Ly6C CD41 CD41 CD61 (Integrin b3) CD61 Platelet CD9 CD62 CD62P (activated platelets) CD235a CD235a Erythrocyte Ter-119 CD146 MECA-32 CD106 CD146 Endothelial Cell CD31 CD62E (activated endothelial cells) Epithelial Cell CD236 CD326 (EPCAM1) For Research Use Only.
    [Show full text]
  • Role of C5ar1 and C5L2 Receptors in Ischemia-Reperfusion Injury
    Journal of Clinical Medicine Article Role of C5aR1 and C5L2 Receptors in Ischemia-Reperfusion Injury Carlos Arias-Cabrales 1,* , Eva Rodriguez-Garcia 1, Javier Gimeno 2, David Benito 3, María José Pérez-Sáez 1, Dolores Redondo-Pachón 1, Anna Buxeda 1, Carla Burballa 1, Marta Crespo 1, Marta Riera 3,* and Julio Pascual 1,* 1 Department of Nephrology, Parc de Salut Mar, 08003 Barcelona, Spain; [email protected] (E.R.-G.); [email protected] (M.J.P.-S.); [email protected] (D.R.-P.); [email protected] (A.B.); [email protected] (C.B.); [email protected] (M.C.) 2 Department of Pathology, Parc de Salut Mar, 08003 Barcelona, Spain; [email protected] 3 Kidney Research Group, Hospital del Mar Medical Research Institute, IMIM, 08003 Barcelona, Spain; [email protected] * Correspondence: [email protected] (C.A.-C.); [email protected] (M.R.); [email protected] (J.P.) Abstract: The role of C5a receptors (C5aR1 and C5L2) in renal ischemia-reperfusion injury (IRI) is uncertain. We generated an in vitro model of hypoxia/reoxygenation with human proximal tubule epithelial cells to mimic some IRI events. C5aR1, membrane attack complex (MAC) and factor H (FH) deposits were evaluated with immunofluorescence. Quantitative polymerase chain reaction evaluated the expression of C5aR1, C5L2 genes as well as genes related to tubular injury, inflammation, and profibrotic pathways. Additionally, C5aR1 and C5L2 deposits were evaluated in kidney graft biopsies (KB) from transplant patients with delayed graft function (DGF, n = 12) and compared with Citation: Arias-Cabrales, C.; a control group (n = 8). We observed higher immunofluorescence expression of C5aR1, MAC and FH Rodriguez-Garcia, E.; Gimeno, J.; as higher expression of genes related to tubular injury, inflammatory and profibrotic pathways and Benito, D.; Pérez-Sáez, M.J.; of C5aR1 in the hypoxic cells; whereas, C5L2 gene expression was unaffected by the hypoxic stimulus.
    [Show full text]
  • The Membrane Complement Regulatory Protein CD59 and Its Association with Rheumatoid Arthritis and Systemic Lupus Erythematosus
    Current Medicine Research and Practice 9 (2019) 182e188 Contents lists available at ScienceDirect Current Medicine Research and Practice journal homepage: www.elsevier.com/locate/cmrp Review Article The membrane complement regulatory protein CD59 and its association with rheumatoid arthritis and systemic lupus erythematosus * Nibhriti Das a, Devyani Anand a, Bintili Biswas b, Deepa Kumari c, Monika Gandhi c, a Department of Biochemistry, All India Institute of Medical Sciences, New Delhi 110029, India b Department of Zoology, Ramjas College, University of Delhi, India c University School of Biotechnology, Guru Gobind Singh Indraprastha University, India article info abstract Article history: The complement cascade consisting of about 50 soluble and cell surface proteins is activated in auto- Received 8 May 2019 immune inflammatory disorders. This contributes to the pathological manifestations in these diseases. In Accepted 30 July 2019 normal health, the soluble and membrane complement regulatory proteins protect the host against Available online 5 August 2019 complement-mediated self-tissue injury by controlling the extent of complement activation within the desired limits for the host's benefit. CD59 is a membrane complement regulatory protein that inhibits the Keywords: formation of the terminal complement complex or membrane attack complex (C5b6789n) which is CD59 generated on complement activation by any of the three pathways, namely, the classical, alternative, and RA SLE the mannose-binding lectin pathway. Animal experiments and human studies have suggested impor- Pathophysiology tance of membrane complement proteins including CD59 in the pathophysiology of rheumatoid arthritis Disease marker (RA) and systemic lupus erythematosus (SLE). Here is a brief review on CD59 and its distribution, structure, functions, and association with RA and SLE starting with a brief introduction on the com- plement system, its activation, the biological functions, and relations of membrane complement regu- latory proteins, especially CD59, with RA and SLE.
    [Show full text]
  • Changes to the Technical Manual, 18Th Edition Monday, November 17, 2014 12:00 P.M
    Changes to the Technical Manual, 18th Edition Monday, November 17, 2014 12:00 p.m. – 1:30 p.m. (ET) / 5:00p.m. – 6:30 p.m. (GMT) When this file is opened, Acrobat Reader will, by default, display the slides including the Acrobat reader controls. To return to full screen mode, hit Ctrl-L on your computer keyboard or use your mouse to click View>Full Screen on the menu bar of the Acrobat Reader program. To take the slides out of full screen mode and display the Acrobat Reader controls, simply hit the Esc key on your computer keyboard. To advance slides during the program, use the Enter, Page Down, down arrow or right arrow on your computer keyboard. To back up slides during the program, use the Page Up, up arrow of left arrow on your computer keyboard. Please remember to logon to the Live Learning Center using your email address and password to complete an evaluation of the program and speakers. At this time, advance to the next slide and wait for the audioconference to begin. A 2014 Audioconference presented to you by AABB The AABB Technical Manual 18th Edition What’s new? www.aabb.org Technical Manual by the Numbers • 1953 =year of first edition • 69 = number of authors/editors this edition • 370,378 = word count • 96 = number of methods • 60 = number of countries where TM is used www.aabb.org It’s a Process www.aabb.org Overview of Changes Major • Molecular testing • Patient blood management • Cellular therapy • Methods Minor • Throughout www.aabb.org 1: Quality Systems 2: Facilities and Safety • These 2 chapters are comprehensive discussions
    [Show full text]
  • An Anticomplement Agent That Homes to the Damaged Brain and Promotes Recovery After Traumatic Brain Injury in Mice
    An anticomplement agent that homes to the damaged brain and promotes recovery after traumatic brain injury in mice Marieta M. Rusevaa,1,2, Valeria Ramagliab,1, B. Paul Morgana, and Claire L. Harrisa,3 aInstitute of Infection and Immunity, School of Medicine, Cardiff University, Cardiff CF14 4XN, United Kingdom; and bDepartment of Genome Analysis, Academic Medical Center, Amsterdam 1105 AZ, The Netherlands Edited by Douglas T. Fearon, Cornell University, Cambridge, United Kingdom, and approved September 29, 2015 (received for review July 15, 2015) Activation of complement is a key determinant of neuropathology to rapidly and specifically inhibit MAC at sites of complement and disability after traumatic brain injury (TBI), and inhibition is activation, and test its therapeutic potential in experimental TBI. neuroprotective. However, systemic complement is essential to The construct, termed CD59-2a-CRIg, comprises CD59a linked fight infections, a critical complication of TBI. We describe a to CRIg via the murine IgG2a hinge. CD59a prevents assembly targeted complement inhibitor, comprising complement receptor of MAC in cell membranes (16), whereas CRIg binds C3b/iC3b of the Ig superfamily (CRIg) fused with complement regulator CD59a, deposited at sites of complement activation (17). The IgG2a designed to inhibit membrane attack complex (MAC) assembly at hinge promotes dimerization to increase ligand avidity. CD59- sites of C3b/iC3b deposition. CRIg and CD59a were linked via the 2a-CRIg protected in the TBI model, demonstrating that site- IgG2a hinge, yielding CD59-2a-CRIg dimer with increased iC3b/C3b targeted anti-MAC therapeutics may be effective in prevention binding avidity and MAC inhibitory activity. CD59-2a-CRIg inhibited of secondary neuropathology and improve neurologic recovery MAC formation and prevented complement-mediated lysis in vitro.
    [Show full text]
  • Blood Product Modifications: Leukofiltration, Irradiation and Washing
    Blood Product Modifications: Leukofiltration, Irradiation and Washing 1. Leukocyte Reduction Definitions and Standards: o Process also known as leukoreduction, or leukofiltration o Applicable AABB Standards, 25th ed. Leukocyte-reduced RBCs At least 85% of original RBCs < 5 x 106 WBCs in 95% of units tested . Leukocyte-reduced Platelet Concentrates: At least 5.5 x 1010 platelets in 75% of units tested < 8.3 x 105 WBCs in 95% of units tested pH≥6.2 in at least 90% of units tested . Leukocyte-reduced Apheresis Platelets: At least 3.0 x 1011 platelets in 90% of units tested < 5.0 x 106 WBCs 95% of units tested pH≥6.2 in at least 90% of units tested Methods o Filter: “Fourth-generation” filters remove 99.99% WBCs o Apheresis methods: most apheresis machines have built-in leukoreduction mechanisms o Less efficient methods of reducing WBC content . Washing, deglycerolizing after thawing a frozen unit, centrifugation . These methods do not meet requirement of < 5.0 x 106 WBCs per unit of RBCs/apheresis platelets. Types of leukofiltration/leukoreduction o “Pre-storage” . Done within 24 hours of collection . May use inline filters at time of collection (apheresis) or post collection o “Pre-transfusion” leukoreduction/bedside leukoreduction . Done prior to transfusion . “Bedside” leukoreduction uses gravity-based filters at time of transfusion. Least desirable given variability in practice and absence of proficiency . Alternatively performed by transfusion service prior to issuing Benefits of leukoreduction o Prevention of alloimmunization to donor HLA antigens . Anti-HLA can mediate graft rejection and immune mediated destruction of platelets o Leukoreduced products are indicated for transplant recipients or patients who are likely platelet transfusion dependent o Prevention of febrile non-hemolytic transfusion reactions (FNHTR) .
    [Show full text]
  • Flow Reagents Single Color Antibodies CD Chart
    CD CHART CD N° Alternative Name CD N° Alternative Name CD N° Alternative Name Beckman Coulter Clone Beckman Coulter Clone Beckman Coulter Clone T Cells B Cells Granulocytes NK Cells Macrophages/Monocytes Platelets Erythrocytes Stem Cells Dendritic Cells Endothelial Cells Epithelial Cells T Cells B Cells Granulocytes NK Cells Macrophages/Monocytes Platelets Erythrocytes Stem Cells Dendritic Cells Endothelial Cells Epithelial Cells T Cells B Cells Granulocytes NK Cells Macrophages/Monocytes Platelets Erythrocytes Stem Cells Dendritic Cells Endothelial Cells Epithelial Cells CD1a T6, R4, HTA1 Act p n n p n n S l CD99 MIC2 gene product, E2 p p p CD223 LAG-3 (Lymphocyte activation gene 3) Act n Act p n CD1b R1 Act p n n p n n S CD99R restricted CD99 p p CD224 GGT (γ-glutamyl transferase) p p p p p p CD1c R7, M241 Act S n n p n n S l CD100 SEMA4D (semaphorin 4D) p Low p p p n n CD225 Leu13, interferon induced transmembrane protein 1 (IFITM1). p p p p p CD1d R3 Act S n n Low n n S Intest CD101 V7, P126 Act n p n p n n p CD226 DNAM-1, PTA-1 Act n Act Act Act n p n CD1e R2 n n n n S CD102 ICAM-2 (intercellular adhesion molecule-2) p p n p Folli p CD227 MUC1, mucin 1, episialin, PUM, PEM, EMA, DF3, H23 Act p CD2 T11; Tp50; sheep red blood cell (SRBC) receptor; LFA-2 p S n p n n l CD103 HML-1 (human mucosal lymphocytes antigen 1), integrin aE chain S n n n n n n n l CD228 Melanotransferrin (MT), p97 p p CD3 T3, CD3 complex p n n n n n n n n n l CD104 integrin b4 chain; TSP-1180 n n n n n n n p p CD229 Ly9, T-lymphocyte surface antigen p p n p n
    [Show full text]
  • Quantitation of the Number of Molecules of Glycophorins C and D on Normal Red Blood Cells Using Radioiodinatedfab Fragments of Monoclonal Antibodies
    Quantitation of the Number of Molecules of Glycophorins C and D on Normal Red Blood Cells Using RadioiodinatedFab Fragments of Monoclonal Antibodies By Jon Smythe, Brigitte Gardner, andDavid J. Anstee Two rat monoclonal antibodies (BRAC 1 and BRAC 1 1 ) cytes. Fabfragments of BRAC 1 1 and ERIC 10 gave values have been produced. BRAC 1 recognizes an epitope com- of 143,000 molecules GPC per red blood cell (RBC). Fab mon to the human erythrocyte membrane glycoproteins fragments of BRAC1 gave 225,000 molecules of GPC and glycophorin C (GPC) and glycophorin D (GPD). BRAC 11 GPD per RBC. These results indicate that GPC and GPD is specific for GPC. Fabfragments of these antibodies and together are sufficiently abundantto provide membrane at- BRlC 10, a murine monoclonal anti-GPC,were radioiodin- tachment sites for all ofthe protein 4.1 in normal RBCs. ated and used in quantitative binding assays to measure 0 1994 by The American Societyof Hematology. the number of GPC and GPD molecules on normal erythro- HE SHAPE AND deformability of the mature human (200,000)" and those reported for GPC (50,000).7 This nu- Downloaded from http://ashpublications.org/blood/article-pdf/83/6/1668/612763/1668.pdf by guest on 24 September 2021 T erythrocyte is controlled by a flexible two-dimensional merical differencehas led to the suggestion that a significant lattice of proteins, which together comprise the membrane proportion of protein 4.1 in normal erythrocyte membranes skeleton.' The major components of the skeleton are spec- must be bound to sites other than GPC and GPD.3 The trin, actin, ankyrin, and protein 4.1.
    [Show full text]
  • Guidance for the Provision of Intraoperative Cell Salvage
    Enter Organisation details here GUIDANCE FOR THE PROVISION OF INTRAOPERATIVE CELL SALVAGE Guidance Guidance forfor Australian Australian Health Health Providers Providers MARCH> MARCH 2014 2014 Guidance for the provision of Intraoperative Cell Salvage Page 0 Ref No: Enter Organisation Ref AUS ICS Version No: 1 March 2014 Enter Organisation details here With the exception of any logos and registered trademarks, and where otherwise noted, all material presented in this document is provided under a Creative Commons Attribution 3.0 Australia (http://creativecommons.org/ licenses/by/3.0/au/) licence. The details of the relevant licence conditions are available on the Creative Commons website (accessible using the links provided) as is the full legal code for the CC BY 3.0 AU license (http://creativecommons.org/licenses/by/3.0/au/legalcode). The content obtained from this document or derivative of this work must be attributed as the Guidance for the provision of Intraoperative Cell Salvage. © National Blood Authority, 2014. ISBN 978-0-9873687-3-7 This report is available online at: www.blood.gov.au For more information: Patient Blood Management National Blood Authority Locked Bag 8430 Canberra ACT 2601 Phone: 13000 BLOOD (13 000 25663) Email: [email protected] www.blood.gov.au Guidance for the provision of Intraoperative Cell Salvage Page 1 Ref No: Enter Organisation Ref AUS ICS Version No: 1 March 2014 Enter Organisation details here Guidance for the provision of Intraoperative Cell Salvage Author: Policy ratified by: Responsible Officer: Signature Date Insert Date Classification Clinical Date Issued Area Applicable Review Date Ref No: Version No: Disclaimer When using this document please ensure that the version you are using is the current, in date version by checking on your Organisation’s database for any new versions.
    [Show full text]
  • CD Markers Are Routinely Used for the Immunophenotyping of Cells
    ptglab.com 1 CD MARKER ANTIBODIES www.ptglab.com Introduction The cluster of differentiation (abbreviated as CD) is a protocol used for the identification and investigation of cell surface molecules. So-called CD markers are routinely used for the immunophenotyping of cells. Despite this use, they are not limited to roles in the immune system and perform a variety of roles in cell differentiation, adhesion, migration, blood clotting, gamete fertilization, amino acid transport and apoptosis, among many others. As such, Proteintech’s mini catalog featuring its antibodies targeting CD markers is applicable to a wide range of research disciplines. PRODUCT FOCUS PECAM1 Platelet endothelial cell adhesion of blood vessels – making up a large portion molecule-1 (PECAM1), also known as cluster of its intracellular junctions. PECAM-1 is also CD Number of differentiation 31 (CD31), is a member of present on the surface of hematopoietic the immunoglobulin gene superfamily of cell cells and immune cells including platelets, CD31 adhesion molecules. It is highly expressed monocytes, neutrophils, natural killer cells, on the surface of the endothelium – the thin megakaryocytes and some types of T-cell. Catalog Number layer of endothelial cells lining the interior 11256-1-AP Type Rabbit Polyclonal Applications ELISA, FC, IF, IHC, IP, WB 16 Publications Immunohistochemical of paraffin-embedded Figure 1: Immunofluorescence staining human hepatocirrhosis using PECAM1, CD31 of PECAM1 (11256-1-AP), Alexa 488 goat antibody (11265-1-AP) at a dilution of 1:50 anti-rabbit (green), and smooth muscle KD/KO Validated (40x objective). alpha-actin (red), courtesy of Nicola Smart. PECAM1: Customer Testimonial Nicola Smart, a cardiovascular researcher “As you can see [the immunostaining] is and a group leader at the University of extremely clean and specific [and] displays Oxford, has said of the PECAM1 antibody strong intercellular junction expression, (11265-1-AP) that it “worked beautifully as expected for a cell adhesion molecule.” on every occasion I’ve tried it.” Proteintech thanks Dr.
    [Show full text]