Academic literature on the topic 'Hemophilia – Genetics'

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Journal articles on the topic "Hemophilia – Genetics"

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Knox, David, Christopher Samuel, Janneth Pazmino-Canizares, et al. "The Genetics of Hemophilia: Analysis of Patients at the Hospital for Sick Children, Toronto, Canada." Blood 108, no. 11 (2006): 1040. http://dx.doi.org/10.1182/blood.v108.11.1040.1040.

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Abstract There is great interest in identifying genetic mutations responsible for hemophilia and in determining if/how mutations correlate with disease phenotype. A hemophilia genetic database was created at SickKids in 2004. At the time <40% of hemophiliacs followed by the clinic had been genotyped. Currently mutations have been identified on 194/236 patients (82%) followed in the clinic. From this we are performing genotype/phenotype correlations. Preliminary analysis has revealed the following novel findings: Most mothers of hemophiliacs are carriers; even when there is a no family h
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Lawn, Richard M., and Gordon A. Vehar. "The Molecular Genetics of Hemophilia." Scientific American 254, no. 3 (1986): 48–54. http://dx.doi.org/10.1038/scientificamerican0386-48.

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Iurea, Iasmina-Maria, Emilia Severin, and Alexandra Matei. "Transforming Hemophilia A Care: Insights into New Therapeutic Options." Life 14, no. 12 (2024): 1568. http://dx.doi.org/10.3390/life14121568.

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Hemophilia A is a hereditary bleeding disorder characterized by a deficiency in clotting factor VIII, leading to significant morbidity and a reduced quality of life. This review provides an updated overview of the current understanding of hemophilia A, highlighting its genetic underpinnings and advancements in treatment strategies. A literature review was conducted using various available databases. Relevant studies on hemophilia A, covering genetics and treatment options, were selected and summarized. Recent developments in gene therapy are discussed, showcasing their potential to offer long-
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Badescu, Minerva Codruta, Manuela Ciocoiu, Elena Rezus, et al. "Current Therapeutic Approach to Acute Myocardial Infarction in Patients with Congenital Hemophilia." Life 11, no. 10 (2021): 1072. http://dx.doi.org/10.3390/life11101072.

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Advances in the treatment of hemophilia have made the life expectancy of hemophiliacs similar to that of the general population. Physicians have begun to face age-related diseases not previously encountered in individuals with hemophilia. Treatment of acute myocardial infarction (AMI) is particularly challenging because the therapeutic strategies influence both the patient’s thrombotic and hemorrhagic risk. As progress has been made in the treatment of AMI over the last decade, we performed an in-depth analysis of the available literature, highlighting the latest advances in the therapy of AMI
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Fernández, Raquel M., Ana Peciña, Beatriz Sánchez, et al. "Experience of Preimplantation Genetic Diagnosis for Hemophilia at the University Hospital Virgen Del Rocío in Spain: Technical and Clinical Overview." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/406096.

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Hemophilia A and B are the most common hereditary hemorrhagic disorders, with an X-linked mode of inheritance. Reproductive options for the families affected with hemophilia, aiming at the prevention of the birth of children with severe coagulation disorders, include preimplantation genetic diagnosis (PGD). Here we present the results of our PGD Program applied to hemophilia, at the Department of Genetics, Reproduction and Fetal Medicine of the University Hospital Virgen del Rocío in Seville. A total of 34 couples have been included in our program since 2005 (30 for hemophilia A and 4 for hemo
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Geddes, Valerie A., and Ross T. A. MacGillivray. "The Molecular Genetics of Hemophilia B." Transfusion Medicine Reviews 1, no. 3 (1987): 161–70. http://dx.doi.org/10.1016/s0887-7963(87)70018-2.

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Chuansumrit, Ampaiwan, Werasak Sasanakul, Ian Williams, Anne Goodeve, Praguywan Kadegasem, and Ian Peake. "Comparison of Phenotypic Assessment and Mutation Detection in the Diagnosis of Carrier State in Hemophilia: Identification of 10 Novel Mutations." Blood 104, no. 11 (2004): 4020. http://dx.doi.org/10.1182/blood.v104.11.4020.4020.

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Abstract The carrier state in 54 females (A38, B16) at risk from 35 moderate and severe hemophilia families (A25, B10) in Thailand, was determined. They were classified as obligate (A17, B8) and possible (A21, B8) carriers by history taking. The phenotypic assessment was performed in two subsequent blood samples taken one week apart when they were not pregnant or on birth control pills. Then, molecular genetics among hemophiliac patients were performed. Inversion of intron 22 among 25 hemophilia A patients was initially performed. Then, the mutations were intensively detected by using conforma
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Chudley, Albert E., and James C. Haworth. "Genetic landmarks through philately - hemophilia." Clinical Genetics 56, no. 4 (1999): 279–81. http://dx.doi.org/10.1034/j.1399-0004.1999.560404.x.

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Astermark, Jan, John Schwarz, Sharyne M. Donfield, et al. "Genetic Factors Associated with Inhibitor Development in Hemophilia A: Initial Results From the Hemophilia Inhibitor Genetics Study (HIGS) Combined Cohort." Blood 114, no. 22 (2009): 217. http://dx.doi.org/10.1182/blood.v114.22.217.217.

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Abstract Abstract 217 Introduction: Both genetic and environmental factors have been implicated as potential risk factors for the development of inhibitory factor VIII (FVIII) antibodies. Previous studies suggest that genetic factors are of major importance. The causative FVIII mutation likely sets the stage for inhibitor risk, with other genetic markers important in determining the final outcome. Data suggest that the process of inhibitor development is complex, involving a variety of immune regulatory genes, several of which have the potential to modify risk. Through a collaboration among th
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Kehl, Alexandra, Anita Haug Haaland, Ines Langbein-Detsch, and Elisabeth Mueller. "A SINE Insertion in F8 Gene Leads to Severe Form of Hemophilia A in a Family of Rhodesian Ridgebacks." Genes 12, no. 2 (2021): 134. http://dx.doi.org/10.3390/genes12020134.

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Hemophilia A is the most common coagulation factor disorder in humans and dogs. The disease is characterized by the lack or diminished activity of Factor VIII (FVIII), caused by variants in the F8 gene and inherited as an X chromosomal trait. Two related male Rhodesian Ridgebacks were diagnosed with Hemophilia A due to reduced FVIII activity. The purpose of the study was to determine the genetic cause and give breeding advice for the remaining family members in order to eradicate the variant. By Sanger sequencing a short interspersed nuclear element (SINE) insertion in exon 14 of the F8 gene w
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Dissertations / Theses on the topic "Hemophilia – Genetics"

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Firrman, Jenni Ann. "ENHANCEMENT OF hFVIII ACTIVITY THROUGH LC MODIFICATIONS FOR GENE THERAPY OF HEMOPHILIA A." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/335863.

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Microbiology and Immunology<br>Ph.D.<br>Gene therapy for Hemophilia A (HA) using the recombinant Adeno-associated virus (rAAV) offers an alternative to classic treatment, which consists of FVIII protein infusions. However, due to limitations associated with rAAV and the FVIII protein itself, the end result is a transgene expression below therapeutic limits. One approach to improving the therapeutic value of rAAV gene therapy for HA is to engineer a more active FVIII protein through genetic modifications. Preliminary testing revealed that canine FVIII Light Chain (kLC) enhances coagulation acti
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Holt, Erika Tyne. "Perceptions of Severity of Children's Bleeding Disorders: Impact on Parental Quality of Life and Reproductive Decisions." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1383060340.

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Landin, Linnéa. "Är genterapi medierad av adenoassocierat virus en effektiv och säker behandling mot hemofili A och B ur ett långsiktigt perspektiv? : En systematisk litteraturstudie." Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-98996.

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Bakgrund - Hemofili A och B är X-kromosombundna blödarsjukdomar, som beror på genetiska avvikelser i de gener som kodar för koagulationsfaktor VIII respektive IX. I dagsläget förlitar sig hemofilipatienter på kontinuerliga intravenösa injektioner med faktorkoncentrat, för att förhindra att potentiellt livshotande blödningar uppstår. Genterapi med rekombinanta adeno-associerade virus (AAV) skulle kunna erbjuda ett kurativt behandlingsalternativ, genom införandet av friska arvsanlag i hepatocyter. Syfte - Syftet med den här litteraturstudien var att undersöka huruvida genterapi me
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Tedgård, Ulf. "Prenatal diagnosis of haemophilia psychological, social and ethical aspects /." Malmö : Dept. of Pediatrics, University Hospital of Malmö, University of Lund, 1999. http://catalog.hathitrust.org/api/volumes/oclc/57455671.html.

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Santos, Andrey dos. "Caracterização de aspectos geneticos e imunologicos envolvidos no desenvolvimento de inibidores em hemofilia A e B." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310746.

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Orientador: Margareth Castro Ozelo<br>Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas<br>Made available in DSpace on 2018-08-15T17:29:43Z (GMT). No. of bitstreams: 1 Santos_Andreydos_D.pdf: 4770033 bytes, checksum: 92cd7a4adf25e169140e6fbbb68fe9d2 (MD5) Previous issue date: 2010<br>Resumo: Uma complicação decorrente do tratamento da hemofilia é a formação de anticorpos neutralizadores da atividade coagulante do fator VIII ou IX (inibidores). Diversos fatores estão relacionados com o desenvolvimento desses inibidores em indivíduos com hemofilia, incluindo f
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Gardiner, Courtney Elizabeth Campbell. "Colours of confetti: the role of ABP genes and environmental variables in flower colour polymorphisms of Rhodohypoxis baurii var. confecta." Thesis, 2019. https://hdl.handle.net/10539/29470.

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A dissertation submitted to the Faculty of Science, University of the Witwatersrand, Johannesburg, South Africa in fulfilment of the requirements for the degree of Master of Science, 2019<br>The study of flower colour is a particularly valuable approach to investigating fundamental evolutionary questions such as the maintenance of variation within species, the role of natural selection and genetic drift in maintaining polymorphisms, and how such polymorphisms contribute to biodiversity. Flower colour is a phenotype that is easily measured and it provides a strong indicator of the out
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Lochan, Anneline. "Genetic factors influencing inhibitor development in a cohort of South African Haemophilia A patients." Thesis, 2014.

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Haemophilia A (HA) is a an X-linked bleeding disorder that manifests due to a mutation in the F8 gene encoding the coagulation factor VIII (FVIII) protein. Therapeutic management of HA involves intravenous FVIII infusions which are either plasma derived or recombinant concentrates that are administered to prevent or manage bleeding episodes promptly. A critical complication of repeated FVIII replacement therapy is the production of FVIII neutralising inhibitors which affect the coagulation potential of the replacement therapy, thus compromising the ability to manage bleeding episodes. The gene
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Tseng, Su-Cheng, and 曾淑真. "Genetic analysis of hemophilia in Taiwanese by using Long-Distance PCR and DHPLC." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/86348523368667918572.

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碩士<br>國立臺灣大學<br>分子醫學研究所<br>93<br>Hemophilia A (HA) and hemophilia B (HB), with the deficiency of coagulation factor VIII (FVIII) and IX (FIX) respectively, represent the most common sex-linked inherited bleeding disorders in human. A wide range of different mutations have been identified including the intrachromosomal inversions involving regions in intron 1 and 22 of the FVIII gene as well as many mutation types found in the remaining part of the factor gene, sunch as large and small deletions, insertions, and point mutations. Patients suffering from those disorders and their families bear gr
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Lin, Shu-Rong, and 林淑容. "Molecular characterization of genetic defects of hemophilia a in chinese patients from Taiwan." Thesis, 1993. http://ndltd.ncl.edu.tw/handle/40164540892982001180.

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Lin, Shu-Rung, and 林淑容. "Molecular Characterization of Genetic Defects of Hemophilia A in Chinese patients from Taiwan." Thesis, 1993. http://ndltd.ncl.edu.tw/handle/12392203444017452310.

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碩士<br>國立臺灣大學<br>醫事技術學系<br>81<br>A型血友病乃因第八因子基因異常所引起,利用聚合■鏈反應(polymerase chain reaction;PCR)及直接核酸序列定位(direct Sequencing)等方 法,可以直接分析病人的第八因子基因. 然而第八因子基因相當巨大,本論 文闡述利用電腦程式設計45對PCR所需的引子(oligonucleotide primers) 來放大第八因子基因的每個特定的exon.接著用單股結構多形性(single strand conformation polymorphism;SSCP)及雙去氧指印法(dideoxy fingerprint -ing;ddF)兩種簡單篩檢方法,可偵測出突變的去氧核糖核酸 片段,這兩種方法都是應用單股去氧核糖核酸的特定形狀(distinct conformation)而偵測出核■酸(nucleotide)的突變. 本研究初步利用 SSCP及ddF鑑定出不正常的 DNA片段,這些DNA片段相對應的exon區域再被
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Books on the topic "Hemophilia – Genetics"

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Pieneman, Wouterina Cynthia. Molecular genetics of hemophilia A. University of Leiden, 1998.

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Karen, Bellenir, ed. Genetic disorders sourcebook: Basic information about heritable diseases and disorders such as Down syndrome, PKU, hemophilia, Von Willebrand disease, Gaucher disease, Tay-Sachs disease, and sickle cell disease ... Omnigraphics, 1996.

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International, Symposium on Blood Transfusion (19th 1994 Groningen Netherlands). Hereditary diseases and blood transfusion: Proceedings of the Nineteenth International Symposium on Blood Transfusion, Groningen, 1994. Kluwer Academic, 1995.

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Hoeben, Robert Cornelis. Towards gene therapy for Haemophilia A: Vectors for the expression of blood-clotting factor VIII in vivo. s.n., 1991.

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Potts, D. M. Queen Victoria's gene. Alan Sutton, 1995.

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Potts, D. M. Queen Victoria's gene: Haemophilia and the royal family. Sutton Pub., 1999.

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Vehar, G. A. Molecular Genetics of Hemophilia. Freeman & Company, W. H., 1995.

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Advances in Hemophilia Treatment: From Genetics to Joint Health. Springer International Publishing AG, 2023.

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Rodríguez-Merchán, E. Carlos. Advances in Hemophilia Treatment: From Genetics to Joint Health. Springer International Publishing AG, 2022.

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Hemophilia. Exon Publications, 2021. http://dx.doi.org/10.36255/hemophilia.

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Hemophilia is a rare genetic disorder that affects the blood’s ability to clot, leading to prolonged or spontaneous bleeding. This article provides a comprehensive guide to understanding hemophilia, covering its causes, symptoms, and treatment options. It begins with an introduction to what hemophilia is and explains its impact on the body. The article describes the types of hemophilia, focusing on Hemophilia A and Hemophilia B, and their genetic basis involving mutations in the F8 and F9 genes. It explores how the condition is inherited, emphasizing its X-linked pattern, which primarily affec
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Book chapters on the topic "Hemophilia – Genetics"

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Sanchez-Lara, Pedro A., and Leonard A. Valentino. "Genetics of Hemophilia A and B." In Advances in Hemophilia Treatment. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-93990-8_2.

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Herrmann, F. H., K. Wulff, G. Auerswald, et al. "Factor VII Deficiency: Clinical Manifestation and Molecular Genetics of 718 Subjects with FVII Gene Mutations." In 37th Hemophilia Symposium. Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-73535-9_51.

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Antonarakis, Stylianos E. "The Molecular Genetics of Hemophilia A and B in Man." In Advances in Human Genetics 1. Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0987-1_2.

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Antonarakis, Stylianos E. "Erratum to: The Molecular Genetics of Hemophilia A and B in Man." In Advances in Human Genetics 1. Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0987-1_6.

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Schneppenheim, R., S. Krey, G. Auerswald, et al. "Human Immunodeficiency Virus-Negative ››High-Risk Patients‹‹ with Hemophilia or Severe von Willebrand Disease Type 3: Coincidence or Genetics?" In 30th Hemophilia Symposium Hamburg 1999. Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-18240-2_24.

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Chen, Harold. "Hemophilia A." In Atlas of Genetic Diagnosis and Counseling. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6430-3_114-2.

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Chen, Harold. "Hemophilia A." In Atlas of Genetic Diagnosis and Counseling. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-2401-1_114.

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Astermark, Jan. "Genetic and Environmental Risk Factors for Inhibitor Development." In Textbook of Hemophilia. Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444318555.ch8.

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Astermark, Jan. "Genetic and Environmental Risk Factors for Factor VIII Inhibitor Development." In Textbook of Hemophilia. John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118398258.ch6.

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Marinova, M., Ph Westhofen, M. Watzka, B. Pötzsch, and J. Oldenburg. "Functional Promoter Polymorphism in the VKORC1 Gene is no Major Genetic Determinant for Vitamin K Dependent Coagulation Factor Activity." In 37th Hemophilia Symposium. Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-73535-9_56.

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Conference papers on the topic "Hemophilia – Genetics"

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Antonarakis, E. "The Molecular Genetics of Hemophilia A Stylianos." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643980.

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Hemophilia A is a common X linked hereditary disorder of blood coagulation due to deficiency of factor 8. The gene for factor 8 has been cloned and characterized (Nature 312:326-342, 1984). It is divided into 26 exons and 25 introns and spans 186 kb of DNA. The CGNA is 9 kb and codes for 2351 amino acids. The first 19 amino acids comprise the secretory leader peptide and the mature excreted polypeptide consists of 2332 amino acids. The nucleotide sequence of the exons and the exon-intron junctions is known and the complete amino acid sequence has been deducedSeveral laboratories have used clon
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Suzuki, N., A. Iizuka, T. Nagao, Y. Nakahori, M. Yamada, and Y. Nakagome. "CARRIER DETECTION OF HEMOPHILIA A BY DNA ANALYSIS IN AFFECTED JAPANESE FAMILIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644008.

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Several DNA probes have been isolated to detect Factor VIII gene and a DNA segment which locates veryclose to the gene. They have been successfully used to detect carriers and patients of hemophilia A.We analyzed DNA samples of Japanese population to see whether these probesare also useful for carrier detection of hemophilia A in affected Japanese families, since the size and frequency of allelic fragments detected by a DNA probe are sometimes different in various ethnic groups.A probe of St14 (DXS52) is thought to be one of the best probes for such analysis in Caucasian population because it
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Ibrahim, Eman, and Rana Hanoon. "Detecting Mutations Linked with Hemophilia A and B in Duhok Province." In 4th Scientific Conference on Women’s Health. Hawler Medical University, 2025. https://doi.org/10.15218/crewh.2024.08.

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Background &amp; Objectives: This study aimed to identify mutations associated with hemophilia A and B in patients from Duhok Province, Iraq. The study sought to characterize genetic mutations in FVIII and FIX genes and their impact on disease manifestation. Materials and Methods: Seventy-five hemophiliac patients (62 with hemophilia A, 13 with hemophilia B) and 75 control subjects were included. DNA extraction, PCR amplification of specific gene regions, and sequencing were performed. Results: Several novel mutations were identified, particularly in intron 22 of the FVIII gene and exon 4 of t
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Lillicrap, D., A. R. Giles, J. J. A. Holden, and B. N. White. "THE RELATIVE EFFICACY OF GENETIC ANALYSIS AND COAGULATION TESTING IN THE DIAGNOSIS OF CARRIERS OF HEMOPHILIA A." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644010.

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This study has assessed the relative benefits of restriction fragment length polymorphism (RFLP) linkage and coagulation testing in the diagnosis of carriers of hemophilia A. 221 samples from 55 families have been studied for intragenic and flanking RFLPs. All samples were tested for the Factor VIII intragenic Bell RFLP and for the flanking marker St 14. 83% of obligate carrier females were heterozygous at oneor both of these two polymorphicsites. However, only38% of these women were heterozygous at the intragenic site and might safely be offered prenatal diagnosis using this marker for the he
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Reisner, H. M., E. A. Reisner, D. D. Kostyu, B. C. Lubahn, C. McMillan, and G. C. White. "POSSIBLE ASSOCIATION OF HLA AND Gm WITH THE ALLOIMMUNE RESPONSE TO FVIII." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644021.

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Between 5 and 15% of individuals with severe hemophilia A are at risk of developing inhibitors (alloantibodies) to FVIII. Genetic factors are important in determining risk, but the nature of these factors is poorly defined. The human immune response to a wide variety of antigens has been associated with the HLA and/or Gm loci. Hence, we have investigated polymorphisms at these two loci in hemophilia A patients with and without inhibitors.DATA SET: To date 127 hemophiliacs have been Gm or HLA typed. Forty-eight are inhibitor positive (I+) based on positive FVIII neutralization assays. This repr
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Kojima, T., M. Tanimoto, T. Kamiya, Y. Obata, K. Kurachi, and H. Saito. "ANALYSIS OF FACTOR IX GENE IN NORMAL SUBJECTS AND HEMOPHILIA B PATIENTS IN JAPAN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644077.

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We have examined DNA samples from 25 hemophilia B patients (21 B- patients, 2 BR patients and 2 B+ patients) and 51 normal subjects with molecular probes (pHFIX and 2 genomic fragments). By structural gene analysis, 4 out of 7 patients who developed anti-factor IX antibodies were detected to have gross factor IX gene deletion. Although these four patients showed normal pattern of HPRT gene detected by pCDHPRT, the gene deletions were found to expand more than 34kb including with entire factor IX exons. Quantitative Southern blot analysis of factor IX gene of the patient's family members indica
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Al-Mohannadi, Anjud Khamis, Sara Deola, and Ahmed Malki. "Visualization of Factor Viii with Flow-Cytometry as a tool for Novel Gene Therapy Approach in Hemophilia A." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0164.

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Haemophilia A is a genetic X-linked disorder, characterized by coagulation Factor VIII (FVIII) deficiency and leading to pathological bleedings. The disease occurs at a rate of 1 in 5000 males’ births. The treatment is the administration of plasma-derived or recombinant Factor VIII, which is expensive and leads to the development of inhibitory antibodies in around 40% of patients affected by the severe form of the disease. The disease becomes for these patients as life threatening. In new approaches to treat Haemophilia include gene therapy (GT), cells corrected through genetic modifications a
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Ørstavik, K. H., L. Kornstad, and H. M. Reisner. "LEWIS BLOOD TYPE HAS AN EFFECT ON THE PLASMA CONCENTRATION OF FACTOR VIII." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644062.

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The plasma concentration of factor VIII is influenced by the ABO blood group. Individuals with blood group 0 have a lower concentration of both factor VIII coagulant activity, factor VIII coagulant antigen (VIIICAg) and factor VIII related antigen (VIHRAg) than individuals with group A, B and AB. Thirty percent of the genetic variance of VIIIRAg concentration is due to the ABO blood group. The Lewis substances Lea and Leb are closely related to the A, B and H substances. We therefore examined the effect of the presence of these antigens on the plasma concentration of VIIICAg and VIIIRAg. The m
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