Dr. Thomas Kickler's Papers

Total Page:16

File Type:pdf, Size:1020Kb

Dr. Thomas Kickler's Papers 1. Rock C, Wong BC, Dionne K, et al. Pseudo-outbreak of Sphingomonas and Methylobacterium sp. Associated with Contamination of Heparin-Saline Solution Syringes Used During Bone Marrow Aspiration. Infection control and hospital epidemiology 2016;37:116-7. 2. Lai H, Moore R, Celentano DD, et al. HIV Infection Itself May Not Be Associated With Subclinical Coronary Artery Disease Among African Americans Without Cardiovascular Symptoms. Journal of the American Heart Association 2016;4:e002529. 3. Kakouros N, Nazarian SM, Stadler PB, Kickler TS, Rade JJ. Risk Factors for Nonplatelet Thromboxane Generation After Coronary Artery Bypass Graft Surgery. Journal of the American Heart Association 2016;4:e002615. 4. Streiff MB, Ye X, Kickler TS, et al. A prospective multicenter study of venous thromboembolism in patients with newly-diagnosed high-grade glioma: hazard rate and risk factors. Journal of neuro- oncology 2015;124:299-305. 5. Lai H, Stitzer M, Treisman G, et al. Cocaine Abstinence and Reduced Use Associated With Lowered Marker of Endothelial Dysfunction in African Americans: A Preliminary Study. Journal of addiction medicine 2015;9:331-9. 6. Gavriilaki E, Yuan X, Ye Z, et al. Modified Ham test for atypical hemolytic uremic syndrome. Blood 2015;125:3637-46. 7. Huang X, Shah S, Wang J, et al. Extensive ex vivo expansion of functional human erythroid precursors established from umbilical cord blood cells by defined factors. Molecular therapy : the journal of the American Society of Gene Therapy 2014;22:451-63. 8. Abt NB, Streiff MB, Gocke CB, Kickler TS, Lanzkron SM. Idiopathic Acquired Hemophilia A with Undetectable Factor VIII Inhibitor. Case reports in hematology 2014;2014:484563. 9. Takemoto CM, Streiff MB, Shermock KM, et al. Activated partial thromboplastin time and anti-xa measurements in heparin monitoring: biochemical basis for discordance. American journal of clinical pathology 2013;139:450-6. 10. Kakouros N, Kickler TS, Laws KM, Rade JJ. Hematocrit alters VerifyNow P2Y12 assay results independently of intrinsic platelet reactivity and clopidogrel responsiveness. Journal of thrombosis and haemostasis : JTH 2013;11:1814-22. 11. DeFilippis AP, Oloyede OS, Andrikopoulou E, et al. Thromboxane A(2) generation, in the absence of platelet COX-1 activity, in patients with and without atherothrombotic myocardial infarction. Circulation journal : official journal of the Japanese Circulation Society 2013;77:2786-92. 12. Bembea MM, Schwartz JM, Shah N, et al. Anticoagulation monitoring during pediatric extracorporeal membrane oxygenation. ASAIO journal 2013;59:63-8. 13. Tai H, Lai H, Jani J, Lai S, Kickler TS. HIV infection and cocaine use induce endothelial damage and dysfunction in African Americans. International journal of cardiology 2012;161:83-7. 14. Olson MT, Kickler TS, Lawson JA, et al. Effect of assay specificity on the association of urine 11- dehydro thromboxane B2 determination with cardiovascular risk. Journal of thrombosis and haemostasis : JTH 2012;10:2462-9. 15. Lai H, Gerstenblith G, Fishman EK, et al. Vitamin D deficiency is associated with silent coronary artery disease in cardiovascularly asymptomatic African Americans with HIV infection. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 2012;54:1747-55. 16. Slichter SJ, Bolgiano D, Kao KJ, et al. Persistence of lymphocytotoxic antibodies in patients in the trial to reduce alloimmunization to platelets: implications for using modified blood products. Transfusion medicine reviews 2011;25:102-10. 17. Lynch DR, Jr., Kickler TS, Rade JJ. Recurrent myocardial infarction associated with gefitinib therapy. Journal of thrombosis and thrombolysis 2011;32:120-4. 18. Gluckman TJ, McLean RC, Schulman SP, et al. Effects of aspirin responsiveness and platelet reactivity on early vein graft thrombosis after coronary artery bypass graft surgery. Journal of the American College of Cardiology 2011;57:1069-77. 19. Nazarian SM, Thompson JB, Gluckman TJ, et al. Clinical and laboratory factors associated with shear-dependent platelet hyper-reactivity in patients on chronic aspirin therapy. Thrombosis research 2010;126:379-83. 20. Mehta BM, Kiani AN, Chen C, Jani J, Kickler TS, Petri M. Endogenous thrombin potential in the assessment of hypercoagulability in systemic lupus erythematosus. American journal of hematology 2010;85:83-5. 21. Walker TJ, Nelson LD, Dunphy BW, Anderson DM, Kickler TS. Comparative evaluation of the Iris iQ200 body fluid module with manual hemacytometer count. American journal of clinical pathology 2009;131:333-8. 22. Strouse JJ, Tamma P, Kickler TS, Takemoto CM. D-dimer for the diagnosis of venous thromboembolism in children. American journal of hematology 2009;84:62-3. 23. Kickler TS. Dr William W. Duke: pioneer in platelet research. Jama 2009;301:2267-9. 24. Gluckman TJ, Segal JB, Schulman SP, et al. Effect of anti-platelet factor-4/heparin antibody induction on early saphenous vein graft occlusion after coronary artery bypass surgery. Journal of thrombosis and haemostasis : JTH 2009;7:1457-64. 25. Garibaldi B, Malani R, Yeh HC, et al. Estimating platelet production in patients with HIV-related thrombocytopenia using the immature platelet fraction. American journal of hematology 2009;84:852-4. 26. Asmis LM, Segal JB, Plantinga LC, et al. Heparin-induced antibodies and cardiovascular risk in patients on dialysis. Thrombosis and haemostasis 2008;100:498-504. 27. Savage WJ, Kickler TS, Takemoto CM. Acquired coagulation factor inhibitors in children after topical bovine thrombin exposure. Pediatric blood & cancer 2007;49:1025-9. 28. Hamilton RG, Kickler TS. Bovine hemoglobin (glutamer-250, Hemopure)-specific immunoglobulin G antibody cross-reacts with human hemoglobin but does not lyse red blood cells in vitro. Transfusion 2007;47:723-8. 29. Ganesh SK, Sharma Y, Dayhoff J, et al. Detection of venous thromboembolism by proteomic serum biomarkers. PloS one 2007;2:e544. 30. Williams MS, Kickler TS, Vaidya D, Ng'alla LS, Bush DE. Evaluation of platelet function in aspirin treated patients with CAD. Journal of thrombosis and thrombolysis 2006;21:241-7. 31. Kickler TS, Oguni S, Borowitz MJ. A clinical evaluation of high fluorescent platelet fraction percentage in thrombocytopenia. American journal of clinical pathology 2006;125:282-7. 32. Danowski A, Kickler TS, Petri M. Anti-beta2-glycoprotein I: prevalence, clinical correlations, and importance of persistent positivity in patients with antiphospholipid syndrome and systemic lupus erythematosus. The Journal of rheumatology 2006;33:1775-9. 33. Brotman DJ, Girod JP, Posch A, et al. Effects of short-term glucocorticoids on hemostatic factors in healthy volunteers. Thrombosis research 2006;118:247-52. 34. Williams MS, Vaidya D, Kickler T, Ouyang P. Long-term hormone replacement therapy does not cause increased platelet activation. American heart journal 2005;150:434-8. 35. Slichter SJ, Davis K, Enright H, et al. Factors affecting posttransfusion platelet increments, platelet refractoriness, and platelet transfusion intervals in thrombocytopenic patients. Blood 2005;105:4106-14. 36. Kickler T. From an early National Blood Foundation award to our ongoing studies in fetal and neonatal alloimmune thrombocytopenia. Transfusion 2005;45:64S-6S. 37. Gluckman TJ, Segal JB, Fredde NL, et al. Incidence of antiplatelet factor 4/heparin antibody induction in patients undergoing percutaneous coronary revascularization. The American journal of cardiology 2005;95:744-7. 38. Althaus J, Weir EG, Askin F, Kickler TS, Blakemore K. Chronic villitis in untreated neonatal alloimmune thrombocytopenia: an etiology for severe early intrauterine growth restriction and the effect of intravenous immunoglobulin therapy. American journal of obstetrics and gynecology 2005;193:1100-4. 39. Streiff MB, Segal J, Grossman SA, Kickler TS, Weir EG. ABO blood group is a potent risk factor for venous thromboembolism in patients with malignant gliomas. Cancer 2004;100:1717-23. 40. Kickler TS, Borowitz MJ, Thompson RE, Charintranont N, Law R. Ret-Y a measure of reticulocyte size: a sensitive indicator of iron deficiency anemia. Clinical and laboratory haematology 2004;26:423-7. 41. Kickler T. Fetal and neonatal alloimmune thrombocytopenia. Clinical advances in hematology & oncology : H&O 2004;2:643-4. 42. Grover DS, Atta MG, Eustace JA, Kickler TS, Fine DM. Lack of clinical utility of urine myoglobin detection by microconcentrator ultrafiltration in the diagnosis of rhabdomyolysis. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2004;19:2634-8. 43. Ziai WC, Torbey MT, Kickler TS, Oh S, Bhardwaj A, Wityk RJ. Platelet count and function in spontaneous intracerebral hemorrhage. Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association 2003;12:201-6. 44. Sacher RA, Kickler TS, Schiffer CA, et al. Management of patients refractory to platelet transfusion. Archives of pathology & laboratory medicine 2003;127:409-14. 45. Kickler TS. Why "bloodless medicine" and how should we do it? Transfusion 2003;43:550-1. 46. Campbell-Lee SA, DeSantis-Parsons D, Shirey RS, Kickler TS. Neonatal alloimmune thrombocytopenia due to anti-HPA-5b (Bra). Immunohematology / American Red Cross 2003;19:127-31. 47. Brotman DJ, Segal JB, Jani JT, Petty BG, Kickler TS. Limitations of D-dimer testing in unselected inpatients with suspected venous thromboembolism. The American journal of medicine 2003;114:276-
Recommended publications
  • Names for GLOB (ISBT 028) Blood Group Alleles
    Names for GLOB blood group alleles v2.0 110914 Names for GLOB (ISBT 028) Blood Group Alleles General description: The GLOB system was acknowledged in 2002 when the P or globoside antigen was moved from the 209 collection. The P antigen is the most common neutral glycosphingolipid in the red cell membrane, belongs to the globoseries and has the following structure: GalNAc3Gal4Gal4Glc1 ceramide, also known as globoside (Gb4Cer). The B3GALT3 gene was first reported in 1998 by Amado et al. to be a member of the 1,3-galactosyltransferase gene family and its product given the name 3Gal-T3. It was later shown by Okajima et al. to possess UDP-N-acetyl galactosamine:globotriaosylceramide 3--N-acetylgalactosaminyl- transferase or globoside synthase activity and the gene name changed to B3GALNT1 and its product renamed 3GalNAc-T1. This enzyme is responsible for the final step in the synthesis of the P antigen, the transfer of GalNAc to the terminal Gal of the Pk antigen. The final proof of this was the identification by Hellberg et al. of critical mutations in the B3GALNT1 gene as the genetic k k basis of P1 and P2 , the rare globoside-deficient null phenotypes of the GLOB system. Gene name: GLOB (B3GALNT1) Number of exons: 5 Initiation codon: Exon 5 Stop codon: Exon 5 GenBank #: AB050855 Entrez Gene ID: 26879 Reference allele: Accession number AB050855 Preferred: GLOB*01 (B3GALNT1*01) Acceptable: P if inferred by haemagglutination Amino acid RBC Phenotype Allele name Nucleotide change Exon change GLOB:1 (P+) GLOB*01 Null phenotypes† GLOB:–1 (P–) GLOB*01N.01 202C>T 5 67Stop GLOB:–1 (P–) GLOB*01N.02 292_293insA 5 97fs102Stop GLOB:–1 (P–) GLOB*01N.03 433C>T 5 Arg145Stop GLOB:–1 (P–) GLOB*01N.04 537_538insA 5 180fs182Stop GLOB:–1 (P–) GLOB*01N.05 648A>C 5 Arg216Ser GLOB:–1 (P–) GLOB*01N.06 797A>C 5 Glu266Ala GLOB:–1 (P–) GLOB*01N.07 811G>A 5 Gly271Arg Page 1 of 2 Names for GLOB blood group alleles v2.0 110914 GLOB:–1 (P–) GLOB*01N.08 959G>A 5 Trp320Stop † k k The null phenotype caused by these alleles can either be P1+ or P1–, i.e.
    [Show full text]
  • Clinical Significance of Antibodies to Antigens in the Raph, John Milton
    R EVIEW Proceedings from the International Society of Blood Transfusion Working Party on Immunohaematology, Workshop on the Clinical Significance of Red Blood Cell Alloantibodies, September 2, 2016, Dubai Clinical significance of antibodies to antigens in the Raph, John Milton Hagen, I, Globoside, Gill, Rh-associated glycoprotein, FORS, JR, LAN, Vel, CD59, and Augustine blood group systems M. Moghaddam and A.A. Naghi This article reviews information on the clinical significance and 6 shared missense mutation c.511C>T (p.Argl71Cys) as of antibodies to antigens in the Raph, John Milton Hagen, I, well as a synonymous single-nucleotide mutation (c.579A>G) Globoside, Gill, Rh-associated glycoprotein, FORS, JR, LAN, Vel, and had no clinical features. Although the CD151 protein is CD59, and Augustine blood group systems. Antibodies to many of the antigens in these groups are rarely encountered because of the critical to cell adhesion and signaling and is implicated in high prevalence of the associated antigens in most populations. cancer progression, its significance in transfusion medicine is For many of these antibodies, the clinical significance—that is, limited to only one report of a hemolytic transfusion reaction the potential to cause reduced survival of transfused antigen- 3 positive red blood cells or a transfusion reaction (e.g., anti-P, (HTR). Least-incompatible RBC units should be selected anti-Jra, and anti-Lan), and/or hemolytic disease of the fetus and for transfusion to patients with anti-MER2.2 No information newborn (e.g., anti-RHAG4 and anti-Vel)—has been documented. on anti-MER2 causing hemolytic disease of the fetus and For other antibodies, their prevalence is so rare that information newborn (HDFN) is available.4 on the clinical significance of their antibodies is not available (e.g., anti-FORS1).
    [Show full text]
  • A Rare Blood Group Phenotype
    Central Journal of Hematology & Transfusion Bringing Excellence in Open Access Case Report *Corresponding author Aisha Mahesar, Department of Hematology, Chughtai K Lab, 10th Jail Road, Gulberg III, Lahore, Pakistan, Tel: P : A Rare Blood Group 0092-331-3760-235; Email: 1 Submitted: 29 December 2017 Accepted: 29 January 2018 Phenotype Published: 30 January 2018 Aisha Mahesar1,2*, Ayisha Imran1, and Noman A. Malik1 ISSN: 2333-6684 1Department of Hematology, Chughtai Lab, Pakistan Copyright 2Department of Blood Bank, Chughtai Lab, Pakistan © 2018 Mahesar et al. OPEN ACCESS Abstract Keywords P blood group antigen of the GLOB system is a glycolipid structure, also known • P blood group as globoside on the Red Blood Cells (RBCs) of almost all individuals worldwide. P1PK • Donath landsteiner antibody blood group system antigens include P , P and PK antigens. Among these, P K phenotype 1 1 • P K phenotype is very rare and the RBCS of these individuals express P1, PK antigens. The high 1 incidence antigen, P, is missing and anti-P antibody is present in the serum. Naturally occurring anti-P is present in the serum of individuals with the rare globoside-deficient k k phenotypes p, P1 , and P2 and has been implicated in hemolytic transfusion reactions, Donath-Landsteiner antibody as well as unfavorable outcomes of pregnancy. When an individual with P1K phenotype needs blood transfusion, they can receive only autologous blood or blood from another P1K phenotype or p phenotype (if P1K blood is not available). We report a case of a young boy with P1K phenotype, anti-P and px2 antibodies who developed a severe hemolytic transfusion reaction and were successfully treated conservatively.
    [Show full text]
  • Studies on the Genetic Basis of Pk, P and P1 Blood Group Antigen Expression Hellberg
    Studies on the genetic basis of Pk, P and P1 blood group antigen expression Hellberg, Åsa 2007 Link to publication Citation for published version (APA): Hellberg, Å. (2007). Studies on the genetic basis of Pk, P and P1 blood group antigen expression. Department of Laboratory Medicine, Lund University. Total number of authors: 1 General rights Unless other specific re-use rights are stated the following general rights apply: Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights. • Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal Read more about Creative commons licenses: https://creativecommons.org/licenses/ 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. LUND UNIVERSITY PO Box 117 221 00 Lund +46 46-222 00 00 Download date: 01. Oct. 2021 Studies on the Genetic Basis of Pk, P and P1 Blood Group Antigen Expression Doctoral thesis by Åsa Hellberg Division of Hematology and Transfusion Medicine Department of Laboratory Medicine Lund University, Sweden With the approval of the Faculty of Medicine at Lund University, this thesis will be defended on March 16, 2007, at 13:00 in Segerfalksalen, Wallenberg Neurocentrum, BMC, Sölvegatan 17, Lund.
    [Show full text]
  • An Update on the GLOB Blood Group System and Collection
    R EVIEW An update on the GLOB blood group system and collection Å. Hellberg, J.S. Westman, and M.L. Olsson The P blood group antigen of the GLOB system is a glycolipid group system (as antigen no. 003002), which is the former structure, also known as globoside, on the red blood cells (RBCs) name of what is now known as the P1PK system (ISBT no. of almost all individuals worldwide. The P antigen is intimately 003), today housing the P1, Pk, and NOR antigens. Thereafter, related to the Pk and NOR antigens discussed in the review about the P1PK blood group system. Naturally occurring anti-P P was moved to the GLOB blood group collection (ISBT no. is present in the serum of individuals with the rare globoside- 209, antigen no. 209001) when it was clear that P1 and P deficient phenotypes p, P k, and P k and has been implicated in 1 2 were only distant relatives. Finally, it was promoted to form hemolytic transfusion reactions as well as unfavorable outcomes of pregnancy. The molecular genetic basis of globoside deficiency a blood group system of its own when the molecular genetic is absence of functional P synthase as a result of mutations basis for P antigen synthesis was established in 2002 (antigen at the B3GALNT1 locus. Other related glycolipid structures, no. 028001).4 Other names sometimes used instead of P, the LKE and PX2 antigens, remain in the GLOB blood group especially in the biochemical and glycobiological literature, collection pending further evidence about the genes and gene products responsible for their synthesis.
    [Show full text]
  • International Society of Blood Transfusion Working Party on Red Cell Immunogenetics and Blood Group Terminology: Cancun Report (2012)
    Vox Sanguinis (2014) 107, 90–96 © 2013 International Society of Blood Transfusion SHORT REPORT DOI: 10.1111/vox.12127 International Society of Blood Transfusion Working Party on red cell immunogenetics and blood group terminology: Cancun report (2012) J. R. Storry,1 L. Castilho,2 G. Daniels,3 W. A. Flegel,4 G. Garratty,5 M. de Haas,6 C. Hyland,7 C. Lomas-Francis,8 J. M. Moulds,9 N. Nogues,10 M. L. Olsson,11 J. Poole,3 M. E. Reid,8 P. Rouger,12 E. van der Schoot,4 M. Scott,3 Y. Tani,13 L.-C. Yu,14 S. Wendel,15 C. Westhoff,8 V. Yahalom16 & T. Zelinski17 1Clinical Immunology and Transfusion Medicine, University and Regional Laboratories, Lund, Sweden 2University of Campinas/Hemocentro, Campinas, Brazil 3Bristol Institute for Transfusion Sciences and IBGRL, NHSBT, Bristol, UK 4Clinical Center, Department of Transfusion Medicine, Bethesda, MD, USA 5American Red Cross Blood Services, Pomona, CA, USA 6Sanquin Blood Supply, Diagnostic Services, Amsterdam, the Netherlands 7Australian Red Cross Blood Services, Brisbane, Australia 8New York Blood Center, New York, NY, USA 9LifeShare Blood Centers, Shreveport, LA, USA 10Banc de Sang i Teixits, Barcelona, Spain 11Department of Laboratory Medicine, Division of Haematology and Transfusion Medicine, Lund University, Sweden 12Centre national de Reference pour les Groupes sanguines, Paris, France 13Japanese Red Cross Kinki Block Blood Center, Ibaraki, Japan 14Mackay Memorial Hospital and National Taiwan University, Taipei, Taiwan 15Blood Bank, Hospital Sirio-Libanes, Sao~ Paulo, Brazil 16NBGRL Magen David Adom, Ramat Gan, Israel 17Rh Laboratory, Winnipeg, Manitoba, Canada The International Society of Blood Transfusion Working Party on red cell immuno- genetics and blood group terminology convened during the International congress in Cancun, July 2012.
    [Show full text]
  • Autocrine IFN Signaling Inducing Profibrotic Fibroblast Responses By
    Downloaded from http://www.jimmunol.org/ by guest on September 23, 2021 Inducing is online at: average * The Journal of Immunology , 11 of which you can access for free at: 2013; 191:2956-2966; Prepublished online 16 from submission to initial decision 4 weeks from acceptance to publication August 2013; doi: 10.4049/jimmunol.1300376 http://www.jimmunol.org/content/191/6/2956 A Synthetic TLR3 Ligand Mitigates Profibrotic Fibroblast Responses by Autocrine IFN Signaling Feng Fang, Kohtaro Ooka, Xiaoyong Sun, Ruchi Shah, Swati Bhattacharyya, Jun Wei and John Varga J Immunol cites 49 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2013/08/20/jimmunol.130037 6.DC1 This article http://www.jimmunol.org/content/191/6/2956.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2013 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 23, 2021. The Journal of Immunology A Synthetic TLR3 Ligand Mitigates Profibrotic Fibroblast Responses by Inducing Autocrine IFN Signaling Feng Fang,* Kohtaro Ooka,* Xiaoyong Sun,† Ruchi Shah,* Swati Bhattacharyya,* Jun Wei,* and John Varga* Activation of TLR3 by exogenous microbial ligands or endogenous injury-associated ligands leads to production of type I IFN.
    [Show full text]
  • From ISBT Terminology Committee, Cape Town
    Names for GLOB (ISBT 028) blood group alleles v3.0 160617 Names for GLOB (ISBT 028) Blood Group Alleles General description: The GLOB system was acknowledged in 2002 when the P or globoside antigen was moved from the 209 collection. The P antigen is the most common neutral glycosphingolipid in the red cell membrane, belongs to the globoseries and has the following structure: GalNAcβ3Galα4Galβ4Glcβ1 ceramide, also known as globoside (Gb4Cer). The B3GALT3 gene was first reported in 1998 by Amado et al. to be a member of the β1,3-galactosyltransferase gene family and its product given the name β3Gal-T3. It was later shown by Okajima et al. to possess UDP-N-acetyl galactosamine:globotriaosylceramide 3-β-N-acetylgalactosaminyl- transferase or globoside synthase activity and the gene name changed to B3GALNT1 and its product renamed β3GalNAc-T1. This enzyme is responsible for the final step in the synthesis of the P antigen, the transfer of GalNAc to the terminal Gal of the Pk antigen. The final proof of this was the identification by Hellberg et al. of critical mutations in the B3GALNT1 gene as the genetic k k basis of P1 and P2 , the rare globoside-deficient null phenotypes of the GLOB system. Gene name: GLOB (B3GALNT1) Number of exons: 5 Initiation codon: Exon 5 Stop codon: Exon 5 Entrez Gene ID: 26879 LRG sequence: NG_007854.1 (genomic) NM_033169.2 (transcript) Reference allele: GLOB*01 (B3GALNT1*01) Acceptable: P if inferred by haemagglutination Reference allele GLOB*01 encodes P Phenotype Allele name Nucleotide change Exon Predicted amino
    [Show full text]
  • Isoantigenic Expressionof Forssman Glycolipid in Human Gastric and Colonic Mucosa
    Proc. Natl. Acad. Sci. USA Vol. 74, No. 7, pp. 3023-3027, July 1977 Medical Sciences Isoantigenic expression of Forssman glycolipid in human gastric and colonic mucosa: Its possible identity with "A-like antigen" in human cancer (Forssman-positive and Forssman-negative populations/tumor/globoside/blood group) S. HAKOMORI, S.-M. WANG, AND W. W. YOUNG, JR. Division of Biochemical Oncology, Fred Hutchinson Cancer Research Center; and Departments of Pathobiology and Microbiology, University of Washington, Seattle, Washington 98104 Communicated by Philip Levine, May 4, 1977 ABSTRACT The heterogenetic Forssman antigen is a gly- and blood group A antigens (5, 6), the A-like activity observed cosphingolipid, a ceramide pentasaccharide with the structure in those studies could have been due to the presence of a GalNAcal-s-3GalNAc,1-a3Galal---4Gal,1--.4Glc-.ceramide. Forssman antigen. In fact, Kawanami (7) described the presence Forssman-positive animals are capable of synthesizing this compound in tissues or in erythrocytes, in contrast to the of Forssman glycolipid in one case of gastric cancer although Forssman-negative species, including humans, which are in- the glycolipid composition of normal mucosa was not examined. capable of adding the last carbohydrate in the sequence of the Consequently, a thorough study has been undertaken using the Forssman antigen, namely aGalNAc. The Forssman glycolipid surgical samples collected by one of the authors (S.M.W.) in and its precursor globoside were examined in twenty-one sam- Taiwan, where there is a high incidence of gastric cancer. ples of surgically extirpated gastrointestinal mucosa and tumors derived therefrom. The results revealed that a few patients had The heterogenetic Forssman antigen (8) is a glycosphingo- chemically and immunologically detectable levels of the lipid (9, 10) whose structure was identified as GalN- Forssman glycolipid as a normal component of their gastroin- Acal1-3GalNAc/ll-3Gala1-'"4Galfll1-'4Glc--ceramide (11, testinal mucosa (F+ population); in contrast, the majority of 12).
    [Show full text]
  • Seltene Bluttypen Und Antikörper Gegen Hochfrequente Erythrozytenantigene
    Seltene Bluttypen und Antikörper gegen hochfrequente Erythrozytenantigene Christof Jungbauer, ÖGBT 2013 Austrian Red Cross, Blood Service Content 1 Introduction 2 Antibody specificities to high frequency antigens: incidence in Europe 3 Impact of migration 4 Supply of rare blood Austrian Red Cross, Blood Service 2 Patients with red cell antibodies Prevalence of the compatible blood type Two situations may challenge an adequate blood supply: • Multiple antibody specificities e.g., anti-e, -Fy a, -Jk a (compatible blood: 1:670) • Specificity to a high frequency antigen (HFA) e.g., anti-k (compatible blood: 1:500) e.g., anti-Kp b (compatible blood: 1:10.000) Austrian Red Cross, Blood Service 3 Patients with red cell antibodies Prevalence of the compatible blood type Two situations may challenge an adequate blood supply: • Multiple antibody specificities e.g., anti-e, -Fy a, -Jk a (compatible blood: 1:670) • Specificity to a high frequency antigen (HFA) e.g., anti-U Blacks 1: 50 Caucasians 1: >10.000 Austrian Red Cross, Blood Service 4 Patients with red cell antibodies Prevalence of the compatible blood type Some (rare) blood types have an unequal prevalence in different ethnic populations While blood establishments have some preparedness for the “local” specificities to HFA, .... reagents and compatible donors for the supply of “exotic” rare blood types are missing Austrian Red Cross, Blood Service 5 modified from: http://www.isbtweb.org/fileadmin/user_upload/WP_on_Red_Cell_Immunogenetics_and/ ISBT BLOOD GROUP SYSTEMS Table_of_blood_group_antigens_within_systems_v2.0_110914.pdf
    [Show full text]
  • SPECIFICATION SPN214/4 the Clinical Significance of Blood Group Alloantibodies and the Supply of Blood for Transfusion Copy Numb
    SPECIFICATION SPN214/4 The Clinical Significance of Blood Group Alloantibodies and the Supply of Blood for Transfusion This Specification replaces Copy Number SPN214/3 Effective 03/05/17 Summary of Significant Changes Change of author to Nicole Thornton from Geoff Daniels (retired). Update to blood group systems (new systems added) Update to some rare antibodies due to availability of new data Change of regional coordinators and associated contact information Removal of unnecessary information to improve clarity Purpose This document outlines current knowledge on the clinical significance of blood group alloantibodies. Its prime purpose is to enable clinical decisions to be made regarding the management and blood transfusion support of patients with blood group antibodies that are not commonly encountered and for which antigen-negative blood is not available in the routine stock. The overall aim is to ensure that a uniform RCI Clinical Policy for the supply of blood for transfusion is implemented throughout the NHSBT. Definitions BSH British Committee for Standards in IAT Indirect Antiglobulin Test Haematology IBGRL International Blood Group DHTR Delayed Haemolytic Transfusion Reference Laboratory Reaction IRDP International Rare Donor Panel HDFN Haemolytic Disease of the Fetus NHSBT NHS Blood and Transplant and Newborn NFBB National Frozen Blood Bank HTR Haemolytic Transfusion Reaction RCI Red Cell Immunohaematology Applicable Documents ESD121 Guidelines for pre-transfusion INF1302: HGP project – targets, phenotype compatibility procedures
    [Show full text]
  • ISBT Science Series
    Science Series INTRODUCTION TO BLOOD TRANSFUSION: FROM DONOR TO RECIPIENT rstar @pikisupe Join the conversation on social media with the hashtag #IntrotoBloodTransfusion ISBT Science Series Volume 15 Supplement 1 December 2020 Special issue: Introduction to Blood Transfusion: From Donor to Recipient CONTENTS Volume 15, Number S1, December 2020 Special issue: Introduction to Blood Transfusion: From Donor to Recipient List of contributors………………………………………………………………………….. ............................................................................................. 1 First Edition • Introduction .......................................................................................................................................................................................... 3 Second Edition • Introduction .......................................................................................................................................................................................... 4 • Preface ................................................................................................................................................................................................... 5 Abbreviations ........................................................................................................................................................................................... 6 Glossary ......................................................................................................................................................................................
    [Show full text]