A New Strategy To Identify Rare Blood Donors: Single Polymerase Chain Reaction Multiplex Snapshot Reaction For Detection Of 16 Blood Group Alleles

Background. As an alternative to phenotyping, large-scale DNA-based assays, which are feasible for high-throughput donor red blood cell typing, were developed for determination of blood group polymorphisms. However, high-throughput genotyping platforms based on these technologies are still expensive and the inclusion of single nucleotide polymorphisms and analysis of the alleles depend on the manufacturer's determination. To overcome this limitation and in order to develop an assay to enable the screening of rare donors, we developed a SNaPshot assay for analysis of nine single nucleotide polymorphisms related to antigens that are difficult to assess using conventional serology. Materials and methods. The single polymerase chain reaction multiplex SNaPshot reaction was optimized to identify nine single nucleotide polymorphisms determining 16 alleles: KEL*3/KEL*4, KEL*6/KEL*7, DI*1/DI*2, DI*3/DI*4, YT*1/YT*2, CO*1/CO*2, DO*1/DO*2, DO*4, DO*5. We designed a single multiplex PCR with primers encompassing the blood group single nucleotide polymorphisms and performed an internal reaction with probe primers able to discriminate the alleles after fragment analysis. The SNaPshot assay was validated with 140 known alleles previously determined by PCR restriction fragment length polymorphism. Results. We were able to simultaneous detect nine single nucleotide polymorphisms defining 16 blood group alleles on an assay based on a multiplex PCR combined with a single base extension using genomic DNA. Discussion. This study demonstrates a robust genotyping strategy for conducting rare donor screening which can be applied in blood centers and could be an important tool for identifying antigen-negative donors and, therefore, for providing rare blood. © SIMTI Servizi Srl.12SUPPL.1s256s263Jungbauer, C., Routine use of DNA testing for red cell antigens in blood centres (2011) Transfus Apher Sci, 45, pp. 61-68Nance, S.T., How to find, recruit and maintain rare blood donors (2009) Curr Opin Hematol, 16, pp. 503-508Veldhuisen, B., Van Der Schoot, C.E., De Haas, M., Blood group genotyping: From patient to high-throughput donor screening (2009) Vox Sang, 97, pp. 198-206Moulds, J.M., Future of molecular testing for red blood cell antigens (2010) Clin Lab Med, 30, pp. 419-429Patnaik, S.K., Helmberg, W., Blumenfeld, O.O., BGMUT: NCBI dbRBC database of allelic variations of genes encoding antigens of blood group systems (2012) Nucleic Acids Res, 40, pp. D1023-D1029Vallone, P.M., Butler, J.M., AutoDimer: A screening tool for primer-dimer and hairpin structures (2004) Biotechniques, 37, pp. 226-231Baleotti Jr., W., Rios, M., Reid, M.E., Dombrock gene analysis in Brazilian people reveals novel alleles (2006) Vox Sang, 91, pp. 81-87Rios, M., Hue-Roye, K., Oyen, R., Insights into the Holleyand Joseph- phenotypes (2002) Transfusion, 42, pp. 52-58Baleotti Jr., W., Rios, M., Reid, M.E., A novel DI*A allele without the Band 3-Memphis mutation in Amazonian Indians (2003) Vox Sang, 84, pp. 326-330Arnoni, C., Latini, F.R.M., Person, R.M., Padronização das técnicas de PCR-RFLP para genotipagem dos alelos KEL*3/ KEL*4 e KEL*5/KEL*6 (2011) Rev Bras Hematol Hemoter, 33 (SUPPL.2), pp. 332-488Baleotti Jr., W., Suzuki, R.B., Ruiz, M., A PCR-RFLP strategy for Wright typing (2011) Rev Bras Hematol Hemoter, 33 (SUPPL. 2), pp. 332-488Brazilian Real - United States Dollar Exchange Rate from Central Bank of Brazil, , http://www4.bcb.gov.br/pec/taxas, April 1st to April 30th, 27/03/2013Daniels, G., The molecular genetics of blood group polymorphism (2009) Hum Genet, 126, pp. 729-742Logdberg, L., Reid, M.E., Zelinski, T., Human blood group genes 2010: Chromosomal locations and cloning strategies revisited (2011) Transfus Med Rev, 25, pp. 36-46Di Cristofaro, J., Silvy, M., Chiaroni, J., Bailly, P., Single PCR multiplex SNaPshot reaction for detection of eleven blood group nucleotide polymorphisms: Optimization, validation, and one year of routine clinical use (2010) J Mol Diagn, 12, pp. 453-460Ferri, G., Pelotti, S., Multiplex ABO genotyping by minisequencing (2009) Methods Mol Biol, 496, pp. 51-58Palacajornsuk, P., Halter, C., Isakova, V., Detection of blood group genes using multiplex SNaPshot method (2009) Transfusion, 49, pp. 740-749Silvy, M., Simon, S., Gouvitsos, J., Weak D and DEL alleles detected by routine SNaPshot genotyping: Identification of four novel RHD alleles (2011) Transfusion, 51, pp. 401-411Silvy, M., Di Cristofaro, J., Beley, S., Identification of RHCE and KEL alleles in large cohorts of Afro-Caribbean and Comorian donors by multiplex SNaPshot and fragment assays: A transfusion support for sickle cell disease patients (2011) Br J Haematol, 154, pp. 260-270Pastinen, T., Kurg, A., Metspalu, A., Minisequencing: A specific tool for DNA analysis and diagnostics on oligonucleotide arrays (1997) Genome Res, 7, pp. 606-614Syvanen, A.C., From gels to chips: "Minisequencing" primer extension for analysis of point mutations and single nucleotide polymorphisms (1999) Hum Mutat, 13, pp. 1-10Information notebook (2011) Blood and Hemoderivates Brasília, , Ministério da Saúde. Secretaria de Atenção à Saúde. Coordenação-Geral de Sangue e Hemoderivados. Hemotherapy production. Unified Health System - SUS Brazil - (Public and private contractors). Private non-contracted services by Unified Health System (SUS Brazil). 4th edSantos, N.P., Ribeiro-Rodrigues, E.M., Ribeiro-Dos-Santos, A.K., Assessing individual interethnic admixture and population substructure using a 48-insertion-deletion (INSEL) ancestry-informative marker (AIM) panel (2010) Hum Mutat, 31, pp. 184-190Storry, J.R., Human blood groups: Inheritance and importance in transfusion medicine (2003) J Infus Nurs, 26, pp. 367-37

Serologic strategy in detecting RHD altered alleles in Brazilian blood donors

We evaluated different technological approaches and anti-D clones to propose the most appropriate serologic strategy in detecting the largest numbers of D variants in blood donors. Methods: We selected 101 samples from Brazilian blood donors with different expressions of D in our donor routine. The tests were performed in immediate spin (IS) with eleven commercially available anti-D reagents in a tube and microplate. The D confirmatory tests for the presence of weak D included the indirect antiglobulin test (IAT) in a tube, gel and solid-phase red blood cell adherence (SPRCA). All DNA samples were extracted from peripheral blood and the D variants were classified using different molecular assays. Results: The RHD variants identified by molecular analysis included weak D types (1, 2, 3, 11 and 38) and partial Ds (DAR1.2, DAR1, DAR3.1, DAU0, DAU2, DAU4, DAU5, DAU6, DMH and DVII). The monoclonal-monoclonal blend RUM-1/MS26 was the best anti-D reagent used in detecting the D antigen in the IS phase in a tube, reacting with 83.2% of the D variants, while the anti-D blend D175 + 415 was the best monoclonal antibody (MoAb) used in a microplate to minimize the need for an IAT, reacting with 83.2% of the D variants. The D confirmatory tests using SPRCA showed a reactivity (3 - 4+) with 100% of the D variant samples tested. Conclusion: Our results show that, even using sensitive methods and MoAbs to ensure the accurate assignment of the D antigen, at least 17% of our donor samples need a confirmatory D test in order to avoid alloimmunization in D-negative patientssem informaçãosem informaçã

Darc (duffy) And Bcam (lutheran) Reduced Expression In Thyroid Cancer

Duffy or DARC (Duffy Antigen Receptor for Chemokines) is a glycosylated membrane protein that selectively binds angiogenic chemokines. Previous in vivo and in vitro studies of DARC function in cancer have associated DARC over expression with better prognosis, decreased metastatic potential, and inhibition of tumor-associated neovascularization. Another carcinogenesis-associated antigen is Lutheran or BCAM (basal cell adhesion molecule), a surface glycoprotein that acts as a receptor for the extracellular matrix protein, laminin. BCAM is a protein related to tumor progression; and, its over expression is associated with skin, ovarian and pancreatic cancers. We explored DARC and BCAM functions and investigated whether or not their expressions were altered in thyroid cancer. The expression of DARC and BCAM were evaluated by quantitative real-time PCR (qPCR) in a set of 18 normal thyroid tissues (NT), 15 follicular adenomas (FTA), 17 follicular carcinomas (FTC), and 122 papillary thyroid carcinomas (PTC), including 78 classical (CVPTC) and 44 follicular variant (FVPTC). RNA was isolated, reverse transcribed to cDNA, and used in qPCR reactions containing SYBR Green. The relative expression value was calculated using ribosomal protein S8 as an internal control. When we compared benign (NT and FTA) versus malignant samples (FTC, CVPTC and FVPTC) we observed a significant decrease of DARC and BCAM relative expression in malignant cases. Additionally, we correlated clinic-pathological features (tumor size, presence of metastasis, presence of lymphocyte infiltrate) with DARC and BCAM expression. We found a diminished expression of DARC in PTC samples, which was correlated with tumor size and presence of a lymphocyte infiltrate. We, also, found a correlation between decreased BCAM expression and tumor size or presence of metastasis. DARC and BCAM expression was associated with pathogenesis of thyroid carcinoma and correlated with clinical-pathological features. © 2012 Elsevier Inc.503161165Daniels, G., Functions of red cell surface proteins (2007) Vox Sang., 93, pp. 331-340Cartron, J.P., Colin, Y., Structural and functional diversity of blood group antigens (2001) Transfus. Clin. Biol., 8, pp. 163-199Rojewski, M.T., Schrezenmeier, H., Flegel, W.A., Tissue distribution of blood group membrane proteins beyond red cells: evidence from cDNA libraries (2006) Transfus. Apher. Sci., 35, pp. 71-82Garratty, G., Blood group antigens as tumor markers, parasitic/bacterial/viral receptors, and their association with immunologically important proteins (1995) Immunol. Invest., 24, pp. 213-232Mantovani, A., Bonecchi, R., Locati, M., Tuning inflammation and immunity by chemokine sequestration: decoys and more (2006) Nat. Rev. Immunol., 6, pp. 907-918Zeng, X.H., Ou, Z.L., Yu, K.D., Coexpression of atypical chemokine binders (ACBs) in breast cancer predicts better outcomes (2011) Breast Cancer Res. Treat., 125, pp. 715-727Wang, J., Ou, Z.L., Hou, Y.F., Duffy antigen receptor for chemokines attenuates breast cancer growth and metastasis: an experiment with nude mice (2005) Zhonghua Yi Xue Za Zhi, 85, pp. 2033-2037Wang, J., Ou, Z.L., Hou, Y.F., Enhanced expression of Duffy antigen receptor for chemokines by breast cancer cells attenuates growth and metastasis potential (2006) Oncogene, 25, pp. 7201-7211Addison, C.L., Belperio, J.A., Burdick, M.D., Strieter, R.M., Overexpression of the Duffy antigen receptor for chemokines (DARC) by NSCLC tumor cells results in increased tumor necrosis (2004) BMC Cancer, 4, p. 28Sun, G., Wang, Y., Zhu, Y., Huang, C., Ji, Q., Duffy antigen receptor for chemokines in laryngeal squamous cell carcinoma as a negative regulator (2011) Acta Otolaryngol., 131, pp. 197-203Collec, E., Lecomte, M.C., El Nemer, W., Colin, Y., Le Van Kim, C., Novel role for the Lu/BCAM-spectrin interaction in actin cytoskeleton reorganization (2011) Biochem. J., 436, pp. 699-708Kroviarski, Y., El Nemer, W., Gane, P., Direct interaction between the Lu/B-CAM adhesion glycoproteins and erythroid spectrin (2004) Br. J. Haematol., 126, pp. 255-264Bernemann, T.M., Podda, M., Wolter, M., Boehncke, W.H., Expression of the basal cell adhesion molecule (B-CAM) in normal and diseased human skin (2000) J. Cutan. Pathol., 27, pp. 108-111Drewniok, C., Wienrich, B.G., Schon, M., Molecular interactions of B-CAM (basal-cell adhesion molecule) and laminin in epithelial skin cancer (2004) Arch. Dermatol. Res., 296, pp. 59-66Schon, M., Klein, C.E., Hogenkamp, V., Basal-cell adhesion molecule (B-CAM) is induced in epithelial skin tumors and inflammatory epidermis, and is expressed at cell-cell and cell-substrate contact sites (2000) J. Invest. Dermatol., 115, pp. 1047-1053Yu, K.H., Barry, C.G., Austin, D., Stable isotope dilution multidimensional liquid chromatography-tandem mass spectrometry for pancreatic cancer serum biomarker discovery (2009) J. Proteome Res., 8, pp. 1565-1576Nikiforov, Y.E., Nikiforova, M.N., Molecular genetics and diagnosis of thyroid cancer (2011) Nat. Rev. Endocrinol., 7, pp. 569-580Latini, F.R., Hemerly, J.P., Oler, G., Riggins, G.J., Cerutti, J.M., Re-expression of ABI3-binding protein suppresses thyroid tumor growth by promoting senescence and inhibiting invasion (2008) Endocr. Relat. Cancer, 15, pp. 787-799Buckhaults, P., Rago, C., St Croix, B., Secreted and cell surface genes expressed in benign and malignant colorectal tumors (2001) Cancer Res., 61, pp. 6996-7001Cerutti, J.M., Delcelo, R., Amadei, M.J., A preoperative diagnostic test that distinguishes benign from malignant thyroid carcinoma based on gene expression (2004) J. Clin. Invest., 113, pp. 1234-1242Schlumberger, M.J., Papillary and follicular thyroid carcinoma (1998) N. Engl. J. Med., 338, pp. 297-306Muzza, M., Degl'Innocenti, D., Colombo, C., The tight relationship between papillary thyroid cancer, autoimmunity and inflammation: clinical and molecular studies (2010) Clin. Endocrinol. (Oxf), 72, pp. 702-708Kondo, T., Ezzat, S., Asa, S.L., Pathogenetic mechanisms in thyroid follicular-cell neoplasia (2006) Nat. Rev. Cancer, 6, pp. 292-306Dawson, T.C., Lentsch, A.B., Wang, Z., Exaggerated response to endotoxin in mice lacking the Duffy antigen/receptor for chemokines (DARC) (2000) Blood, 96, pp. 1681-1684Planaguma, J., Liljestrom, M., Alameda, F., Matrix metalloproteinase-2 and matrix metalloproteinase-9 codistribute with transcription factors RUNX1/AML1 and ETV5/ERM at the invasive front of endometrial and ovarian carcinoma (2011) Hum. Pathol., 42, pp. 57-67Kikkawa, Y., Sudo, R., Kon, J., Laminin alpha 5 mediates ectopic adhesion of hepatocellular carcinoma through integrins and/or Lutheran/basal cell adhesion molecule (2008) Exp. Cell Res., 314, pp. 2579-2590Le Naour, F., Andre, M., Greco, C., Profiling of the tetraspanin web of human colon cancer cells (2006) Mol. Cell. Proteomics, 5, pp. 845-85

How Do We Identify Rhd Variants Using A Practical Molecular Approach?

Serologic resolution of Rh discrepancies due to partial D or weak D phenotypes is a frequent problem encountered during routine typing that can be solved by RHD genotyping because it provides better characterization of these variants. The objective of the current study was to develop algorithms for identification of D variants in multiethnic populations based on a logic sequence of molecular tests using a large number of atypical RhD specimens. Thus, a total of 360 blood samples with atypical D antigen expression were analyzed. A previously published multiplex polymerase chain reaction (PCR) procedure was performed and depending on multiplex PCR analysis, the associated RHCE allele, and D variant frequency in our population, an algorithm was developed composed of six flow charts using specific PCR-restriction fragment length polymorphism and/or specific exon sequencing. This strategy allowed the identification of 22 different variants with few assays and a much reduced cost. This study describes a simple and practical algorithm that we use to determine RHD genotypes in samples with unknown RHD. This strategy is relatively easy to implement and the algorithm can be adapted to populations with various ethnic backgrounds after an initial assessment of the type and frequency of D variants. Essentially, we demonstrate that sequencing of all RHD exons is not necessary for the identification of the majority of known D variants. © 2013 American Association of Blood Banks.544962969Wagner, F.F., Gassner, C., Muller, T.H., Schonitzer, D., Schunter, F., Flegel, W.A., Flegel, A., Molecular basis of weak D phenotypes (1999) Blood, 93 (1), pp. 385-393Westhoff, C.M., The Structure and Function of the Rh Antigen Complex (2007) Seminars in Hematology, 44 (1), pp. 42-50. , DOI 10.1053/j.seminhematol.2006.09.010, PII S0037196306002320, Transfusion Medicine in the Early 21st CenturyFlegel, W.A., Denomme, G.A., Yazer, M.H., On the complexity of D antigen typing: A handy decision tree in the age of molecular blood group diagnostics (2007) J Obstet Gynaecol Can, 29, pp. 746-752Credidio, D.C., Pellegrino, J., Castilho, L., Serologic and molecular characterization of D variants in Brazilians: Impact for typing and transfusion strategy (2011) Immunohematology, 27, pp. 6-11http://www.isbtweb.org/working-parties/red-cell-immunogenetics-and-blood- group-terminology/blood-group-terminology/blood-group-allele-terminology/, International Society of Blood Transfusion (ISBT) Working Party for Red Cell Immunogenetics and Blood Group Terminology. Blood group allele terminology. [cited 2013 Sep]Flegel, W., (2011) RhesusBase, , http://www.uni-ulm.de/~fwagner/RH/RB/, [cited 2013 Sep]Maaskant-Van Wijk, P.A., Faas, B.H.W., De Ruijter, J.A.M., Overbeeke, M.A.M., Von Dem Borne, A.E.G.K., Van Rhenen, D.J., Van Der Schoot, C.E., Genotyping of RHD by multiplex polymerase chain reaction analysis of six RHD-specific exons (1998) Transfusion, 38 (11-12), pp. 1015-1021Legler, T.J., Maas, J.H., Kohler, M., Wagner, T., Daniels, G.L., Perco, P., Panzer, S., RHD sequencing: A new tool for decision making on transfusion therapy and provision of Rh prophylaxis (2001) Transfusion Medicine, 11 (5), pp. 383-388. , DOI 10.1046/j.1365-3148.2001.00327.xCruz, B.R., Chiba, A.K., Moritz, E., RHD alleles in Brazilian blood donors with weak D or D-negative phenotypes (2012) Transfus Med, 22, pp. 84-89Brajovich, M.E., Boggione, C.T., Biondi, C.S., Comprehensive analysis of RHD alleles in Argentineans with variant D phenotypes (2012) Transfusion, 52, pp. 389-396Fichou, Y., Le Marechal, C., Jamet, D., Establishment of a medium-throughput approach for the genotyping of RHD variants and report of nine novel rare alleles (2013) Transfusion, 53, pp. 1821-1828Wang, D., Lane, C., Quillen, K., Prevalence of RhD variants, confirmed by molecular genotyping, in a multiethnic prenatal population (2010) Am J Clin Pathol, 134, pp. 438-442Granier, T., Beley, S., Chiaroni, J., A comprehensive survey of both RHD and RHCE allele frequencies in sub-Saharan Africa (2013) Transfusion, 53, pp. 3009-3017Kappler-Gratias, S., Auxerre, C., Dubeaux, I., Systematic RH genotyping and variant identification in French donors of African origin (2013) Blood Transfus, 17, pp. 1-8Curtin, P., (1969) Atlantic Slave Trade: A Census, , Milwaukee (WI): University of Wisconsin PressChen, Q., Flegel, W.A., Random survey for RHD alleles among D+ European persons (2005) Transfusion, 45 (7), pp. 1183-1191. , DOI 10.1111/j.1537-2995.2005.00181.xDenomme, G.A., Wagner, F.F., Fernandes, B.J., Partial D, weak D types, and novel RHD alleles among 33,864 multiethnic patients: Implications for anti-D alloimmunization and prevention (2005) Transfusion, 45, pp. 1554-1560Touinssi, M., Chapel-Fernandes, S., Granier, T., Molecular analysis of inactive and active RHD alleles in native Congolese cohorts (2009) Transfusion, 49, pp. 1353-1360Wagner, F.F., Eicher, N.I., Jorgensen, J.R., Lonicer, C.B., Flegel, W.A., DNB: A partial D with anti-D frequent in Central Europe (2002) Blood, 100 (6), pp. 2253-2256. , DOI 10.1182/blood-2002-03-074

An Easy And Efficient Strategy For Kel Genotyping In A Multiethnic Population

Background: The Kell blood group system expresses high and low frequency antigens with the most important in relation to transfusion including the antithetic KEL1 and KEL2; KEL3 and KEL4; KEL6 and KEL7 antigens. Kell is a clinically relevant system, as it is highly immunogenic and anti-KEL antibodies are associated with hemolytic transfusion reactions and hemolytic disease of the fetus and newborn. Although required in some situations, Kell antigen phenotyping is restricted due to technical limitations. In these cases, molecular approaches may be a solution. This study proposes three polymerase chain reaction genotyping protocols to analyze the single nucleotide polymorphisms responsible for six Kell antithetic antigens expressed in a Brazilian population.Methods: DNA was extracted from 800 blood donor samples and three polymerase chain reaction-restriction fragment length polymorphism protocols were used to genotype the KEL*1/KEL*2, KEL*3/KEL*4 and KEL*6/KEL*7 alleles. KEL*3/KEL*4 and KEL*6/KEL*7 genotyping was standardized using the NlalII and MnlI restriction enzymes and validated using sequencing. KEL*1/KEL*2 genotyping was performed using a previously reported assay. Results: KEL genotyping was successfully implemented in the service; the following distribution of KEL alleles was obtained for a population from southeastern Brazil: KEL*1 (22%), KEL*2 (97.8%), KEL*3 (0.69%), KEL*4 (99.31%), KEL*6 (2.69%o) and KEL*7 (9731%o). Additionally, two individuals with rare genotypes, KEL*1/KEL*1 and KEL*3/KEL*3, were identified. Conclusion: KEL allele genotyping using these methods proved to be reliable and applicable to predict Kell antigen expressions in a Brazilian cohort. This easy and efficient strategy can be employed to provide safer transfusions and to help in rare donor screening.35299102(2012), http://www.isbtweb.org, International Society of Blood Transfusion.[Internet].Amsterdam: ISBT, cited 2012 Jun 8Redman, C.M., Avellino, G., Pfeffer, S.R., Mukherjee, T.K., Nichols, M., Rubinstein, P., Kell blood group antigens are part of a 93,000-dalton red cell membrane protein (1986) J Biol Chem, 261 (20), pp. 9521-9525Lee, S., The value of DNA analysis for antigens of the Kell and Kx blood group systems (2007) Transfusion, 47 (SUPPL.1), pp. 32S-39SDaniels, G.L., Anstee, D.J., Cartron, J.P., Dahr, W., Henry, S., Issitt, P.D., Terminology for red cell surface antigens. Makuhari Report (1996) Vox Sang, 71 (4), pp. 246-248Daniels, G.L., Anstee, D.J., Cartron, J.P., Dahr, W., Issitt, P.D., Jorgensen, J., Blood group terminology 1995. ISBT Working Party on terminology for red cell surface antigens (1995) Vox Sang, 69 (3), pp. 265-279Lee, S., Molecular basis of Kell blood group phenotypes (1997) Vox Sang, 73 (1), pp. 1-11. , Erratum in: Vox Sang. 1998;74(1):58Daniels, G., The molecular genetics of blood group polymorphism (2009) Hum Genet, 126 (6), pp. 729-742Westhoff, C.M., Reid, M.E., Review: The Kell, Duffy, and Kidd blood group systems (2004) Immunohematology, 20 (1), pp. 37-49Russo, D., Redman, C., Lee, S., Association of XK and Kell blood group proteins (1998) J Biol Chem, 273 (22), pp. 13950-13956Lee, S., Zambas, E., Green, E.D., Redman, C., Organization of the gene encoding the human Kell blood group protein (1995) Blood, 85 (5), pp. 1364-1370. , . Erratum in: Blood. 1996;87(11):4922Lee, S., Russo, D., Redman, C.M., The Kell blood group system: Kell and XK membrane proteins (2000) Semin Hematol, 37 (2), pp. 113-121Vaughan, J.I., Manning, M., Warwick, R.M., Letsky, E.A., Murray, N.A., Roberts, I.A., Inhibition of erythroid progenitor cells by anti-Kell antibodies in fetal alloimmune anemia (1998) N Engl J Med, 338 (12), pp. 798-803. , Comment in: N Engl J Med. 2000;343(1):72N Engl J Med. 1998;338(12):830-831Duguid, J.K., Bromilow, I.M., Haemolytic disease of the newborn due to anti-k (1990) Vox Sang, 58 (1), p. 69Smoleniec, J., Anderson, N., Poole, G., Hydrops fetalis caused by a blood group antibody usually undetected in routine screening (1994) Arch Dis Child Fetal Neonatal Ed, 71 (3), pp. F216-F217Gorlin, J.B., Kelly, L., Alloimmunisation via previous transfusion places female Kpb-negative recipients at risk for having children with clinically significant hemolytic disease of the newborn (1994) Vox Sang, 66 (1), pp. 46-48Donovan, L.M., Tripp, K.L., Zuckerman, J.E., Konugres, A.A., (1973), 13 (3), p. 153. , Daniels G. Hemolytic disease of the newborn due to anti-Js a. TransfusionStanworth, S., Fleetwood, P., de Silva, M., Severe haemolytic disease of the newborn due to anti-Js(b) (2001) Vox Sang, 81 (2), pp. 134-135Daniels, G., Kell and Kx blood group systems (1995) Human Blood Groups, pp. 385-420. , Oxford: Blackwell ScienceRace, R.R., Sanger, R., (1975) Blood Groups In Man, , 6th ed. Oxford: Blackwell ScientificJungbauer, C., Routine use of DNA testing for red cell antigens in blood centres (2011) Transfus Apher Sci, 45 (1), pp. 61-68Hillyer, C.D., Shaz, B.H., Winkler, A.M., Reid, M., Integrating molecular technologies for red blood cell typing and compatibility testing into blood centers and transfusion services (2008) Transfus Med Rev, 22 (2), pp. 117-132Reid, M.E., Rios, M., Powell, V.I., Charles-Pierre, D., Malavade, V., DNA from blood samples can be used to genotype patients who have recently received a transfusion (2000) Transfusion, 40 (1), pp. 48-53Vallone, P.M., Butler, J.M., AutoDimer: A screening tool for primer-dimer and hairpin structures (2004) Biotechniques, 37 (2), pp. 226-231Santos, N.P., Ribeiro-Rodrigues, E.M., Ribeiro-Dos-Santos, A.K., Pereira, R., Gusmao, L., Amorim, A., Assessing individual interethnic admixture and population substructure using a 48-insertion-deletion (INSEL) ancestry- informative marker (AIM) panel (2010) Hum Mutat, 31 (2), pp. 184-190Renoud, K.J., Barracchini, K., Byrne, K.M., Adams, S., Pickett, A., Caruccio, L., KEL6 and KEL7 genotyping with sequence-specific primers (2006) Transfusion, 46 (9), pp. 1510-151

Two Novel Kel Alleles Encoding K0 Phenotypes In Brazilians

[No abstract available]54821282129Lee, S., Russo, D., Redman, C., Functional and structural aspects of the Kell blood group system (2000) Transfus Med Rev, 14, pp. 93-103Nunn, H.D., Giles, C.M., Dormandy, K.M., A second example of anti-Ku in a patient who has the rare Kell phenotype, Ko (1966) Vox Sang, 11, pp. 611-619Chown, B., Lewis, M., Kaita, K., A new Kell blood-group phenotype (1957) Nature, 180, p. 711Yu, L.C., Twu, Y.C., Chang, C.Y., Molecular basis of the Kell-null phenotype: A mutation at the splice site of human KEL gene abolishes the expression of Kell blood group antigens (2001) J Biol Chem, 276, pp. 10247-10252Lee, S., Russo, D.C., Reiner, A.P., Molecular defects underlying the Kell null phenotype (2001) J Biol Chem, 276, pp. 27281-27289Yang, M.H., Li, L., Kuo, Y.F., Genetic and functional analyses describe a novel 730delG mutation in the KEL gene causing K0 phenotype in a Taiwanese blood donor (2011) Transfus Med, 21, pp. 318-32

Characteristics, management, and outcomes of patients with left‐sided infective endocarditis complicated by heart failure: a substudy of the ESC‐EORP EURO‐ENDO (European infective endocarditis) registry

International audienc