Relevant bibliographies by topics / G6PD: Glucose-6-Phosphate Dehydrogenase Deficiency

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'G6PD: Glucose-6-Phosphate Dehydrogenase Deficiency'

Author: Grafiati
Published: 7 June 2025
Last updated: 2 August 2025

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Journal articles on the topic "G6PD: Glucose-6-Phosphate Dehydrogenase Deficiency"

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Luzzatto, Lucio, Mwashungi Ally, and Rosario Notaro. "Glucose-6-phosphate dehydrogenase deficiency." Blood 136, no. 11 (2020): 1225–40. http://dx.doi.org/10.1182/blood.2019000944.

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Abstract Glucose 6-phosphate dehydrogenase (G6PD) deficiency is 1 of the commonest human enzymopathies, caused by inherited mutations of the X-linked gene G6PD. G6PD deficiency makes red cells highly vulnerable to oxidative damage, and therefore susceptible to hemolysis. Over 200 G6PD mutations are known: approximately one-half are polymorphic and therefore common in various populations. Some 500 million persons with any of these mutations are mostly asymptomatic throughout their lifetime; however, any of them may develop acute and sometimes very severe hemolytic anemia when triggered by inges
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Pes, Giovanni Mario, and Maria Pina Dore. "Acquired Glucose-6-Phosphate Dehydrogenase Deficiency." Journal of Clinical Medicine 11, no. 22 (2022): 6689. http://dx.doi.org/10.3390/jcm11226689.

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Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a hereditary condition caused by mutations on chromosome X and is transmitted by a sex-linked inheritance. However, impairment of G6PD activity may result from biochemical mechanisms that are able to inhibit the enzyme in specific clinical conditions in the absence of a structural gene-level defect. In this narrative review, a number of clinical settings associated with an “acquired” G6PD deficiency, phenotypically undistinguishable from the primary deficiency, as well as the mechanisms involved, were examined. Hyperaldosteronism and diabe
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Ali1, Hind K., and K. A. Shaker2. "GLUCOSE- 6-PHOSPHATE DEHYDROGENASE DEFICIENCY AND FAVISM." iraqi journal of market research and consumer protection 16, no. 1 (2024): 276–85. http://dx.doi.org/10.28936/jmracpc16.1.2024.(24.

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Favism disease, also known as hemolytic syndrome (the breakdown of red blood cells) affects some people (especially male children) when they consume the fava beans (fava bean, broad bean) because they contain high concentrations of pyrimidine glycosides (vicine and convicine) or they take some medications or an imbalance in metabolism or infections. causing the generation of harmful oxygen forms, as these people suffer from a deficiency in the glucose-6-phosphate dehydrogenase (G6PD) enzyme, which is responsible for the availability of, NADPH, which is important in providing reduced glutathion
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Stockham, S. L., J. W. Harvey, and D. A. Kinden. "Equine Glucose-6-phosphate Dehydrogenase Deficiency." Veterinary Pathology 31, no. 5 (1994): 518–27. http://dx.doi.org/10.1177/030098589403100503.

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Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a well-characterized X-linked inherited disorder in humans but has not been reported in horses. We describe a persistent hemolytic anemia and hyperbilirubinemia due to a severe G6PD deficiency in an American Saddlebred colt. Other abnormalities in the colt's erythrocytes as compared with those of healthy horses ( n = 22–35) included increased activities of hexokinase and pyruvate kinase, decreased concentrations of reduced glutathione and reduced nicotinamide adenine dinucleotide phosphate (NADP), and increased concentration of oxidized NA
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Ou, Zilin, Yicong Chen, Jianle Li, et al. "Glucose-6-phosphate dehydrogenase deficiency and stroke outcomes." Neurology 95, no. 11 (2020): e1471-e1478. http://dx.doi.org/10.1212/wnl.0000000000010245.

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ObjectiveTo assess the risk of glucose-6-phosphate dehydrogenase (G6PD) on stroke prognosis, we compared outcomes between patients with stroke with and without G6PD deficiency.MethodsThe study recruited 1,251 patients with acute ischemic stroke. Patients were individually categorized into G6PD-deficiency and non-G6PD-deficiency groups according to G6PD activity upon admission. The primary endpoint was poor outcome at 3 months defined by a modified Rankin Scale (mRS) score ≥2 (including disability and death). Secondary outcomes included the overall mRS score at 3 months and in-hospital death an
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Hecker, Peter A., Jane A. Leopold, Sachin A. Gupte, Fabio A. Recchia, and William C. Stanley. "Impact of glucose-6-phosphate dehydrogenase deficiency on the pathophysiology of cardiovascular disease." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 4 (2013): H491—H500. http://dx.doi.org/10.1152/ajpheart.00721.2012.

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Glucose-6-phosphate dehydrogenase (G6PD) catalyzes the rate-determining step in the pentose phosphate pathway and produces NADPH to fuel glutathione recycling. G6PD deficiency is the most common enzyme deficiency in humans and affects over 400 million people worldwide; however, its impact on cardiovascular disease is poorly understood. The glutathione pathway is paramount to antioxidant defense, and G6PD-deficient cells do not cope well with oxidative damage. Limited clinical evidence indicates that G6PD deficiency may be associated with hypertension. However, there are also data to support a
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Beutler, E., W. Kuhl, JL Vives-Corrons, and JT Prchal. "Molecular heterogeneity of glucose-6-phosphate dehydrogenase A-." Blood 74, no. 7 (1989): 2550–55. http://dx.doi.org/10.1182/blood.v74.7.2550.2550.

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Abstract Glucose-6-phosphate dehydrogenase (G6PD) deficiency is probably the most common disease-producing genetic polymorphism of humans. Virtually all G6PD-deficient Africans show the G6PD A- phenotype, an electrophoretically rapid, deficient enzyme. The recently acquired ability to identify the point mutations producing the different variants has given us new insights into the population genetics of G6PD variants. Twenty-nine males with the G6PD A- phenotype were studied. They were of African, Mexican, Spanish, and US white ethnic origin. All had the A---G transition at nucleotide 376 chara
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Beutler, E., W. Kuhl, JL Vives-Corrons, and JT Prchal. "Molecular heterogeneity of glucose-6-phosphate dehydrogenase A-." Blood 74, no. 7 (1989): 2550–55. http://dx.doi.org/10.1182/blood.v74.7.2550.bloodjournal7472550.

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Glucose-6-phosphate dehydrogenase (G6PD) deficiency is probably the most common disease-producing genetic polymorphism of humans. Virtually all G6PD-deficient Africans show the G6PD A- phenotype, an electrophoretically rapid, deficient enzyme. The recently acquired ability to identify the point mutations producing the different variants has given us new insights into the population genetics of G6PD variants. Twenty-nine males with the G6PD A- phenotype were studied. They were of African, Mexican, Spanish, and US white ethnic origin. All had the A---G transition at nucleotide 376 characteristic
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Yoshida, A., and EF Jr Roth. "Glucose-6-phosphate dehydrogenase of malaria parasite Plasmodium falciparum." Blood 69, no. 5 (1987): 1528–30. http://dx.doi.org/10.1182/blood.v69.5.1528.1528.

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Abstract Plasmodium falciparum growth is impaired in glucose-6-phosphate dehydrogenase (G6PD)-deficient red blood cells (RBCs), and malaria has been implicated in the spreading of deficient variants in malaria- endemic areas. Recent reports suggest that the malaria parasite can adapt itself to grow in these variant RBCs by producing its own G6PD, but studies on parasite G6PD are very limited. In this report, we define the properties of the parasite G6PD. G6PD was partially purified from infected and uninfected variant RBCs associated with severe G6PD deficiency. G6PD from infected RBCs contain
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Yoshida, A., and EF Jr Roth. "Glucose-6-phosphate dehydrogenase of malaria parasite Plasmodium falciparum." Blood 69, no. 5 (1987): 1528–30. http://dx.doi.org/10.1182/blood.v69.5.1528.bloodjournal6951528.

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Plasmodium falciparum growth is impaired in glucose-6-phosphate dehydrogenase (G6PD)-deficient red blood cells (RBCs), and malaria has been implicated in the spreading of deficient variants in malaria- endemic areas. Recent reports suggest that the malaria parasite can adapt itself to grow in these variant RBCs by producing its own G6PD, but studies on parasite G6PD are very limited. In this report, we define the properties of the parasite G6PD. G6PD was partially purified from infected and uninfected variant RBCs associated with severe G6PD deficiency. G6PD from infected RBCs contained two co
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Dissertations / Theses on the topic "G6PD: Glucose-6-Phosphate Dehydrogenase Deficiency"

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Chan, Ting-fai. "An analysis of two naturally occurring G6PD deficient mutants, G6PD Campinus and G6PD Fukaya /." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31370172.

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Chan, Ting-fai, and 陳定輝. "An analysis of two naturally: occurring G6PD deficient mutants, G6PD Campinus and G6PD Fukaya." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31370172.

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Schulte, Seth. "Analysis of Glucose-6-Phosphate Dehydrogenase in Malagasy Males Through Genetic Sequencing and a Population-specific Genotyping Assay." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1459352246.

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Wang, Xiaotao, and 王曉濤. "A comparative study of two recombinant human glucose-6-phosphate dehydrogenase (G6PD) deficient variants with the normal enzyme." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B3122359X.

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Mazulis, Fernando, Claudia Weilg, Urcia Carlos Alberto Alva, Maria J. Pons, and Valle Mendoza Juana Del. "Is glucose-6-phosphate dehydrogenase deficiency more prevalent in Carrion's disease endemic areas in Latin America?" Elsevier B.V, 2015. http://hdl.handle.net/10757/595273.

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Glucose-6-phosphate dehydrogenase (G6PD) is a cytoplasmic enzyme with an important function in cell oxidative damage prevention. Erythrocytes have a predisposition towards oxidized environments due to their lack of mitochondria, giving G6PD a major role in its stability. G6PD deficiency (G6PDd) is the most common enzyme deficiency in humans; it affects approximately 400 million individuals worldwide. The overall G6PDd allele frequency across malaria endemic countries is estimated to be 8%, corresponding to approximately 220 million males and 133 million females. However, there are no reports o
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Wang, Xiaotao, and 王曉濤. "A study of glucose-6-phosphate dehydrogenase (G6PD)class I deficient mutants: R393G and R393H at the dimerinterface versus other mutants." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31451974.

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Wang, Xiaotao. "A study of glucose-6-phosphate dehydrogenase (G6PD)class I deficient mutants R393G and R393H at the dimer interface versus other mutants /." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31451974.

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Ferreira, Maria de Fatima de Carvalho. "Triagem neonatal de deficiência de glicose-6-fosfato desidrogenase e prevalência das mutações G202A (G6PD A-) e C563T (G6PD Mediterrâneo) em Mato Grosso/Brasil." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5141/tde-24102014-115056/.

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Objetivos: A deficiência de glicose-6-fosfato desidrogenase (G6PD) está associada a um maior risco de encefalopatia bilirrubínica e de crise hemolítica aguda grave desencadeada por drogas como a primaquina e a dapsona. Conhecer a prevalência dessa deficiência enzimática em área onde a malária e a hanseníase ainda estão presentes e conhecer a prevalência das principais mutações traz subsídios para planejamento de estratégias com vistas à redução de riscos associados a esta deficiência enzimática. Métodos: Estudo descritivo transversal conduzido em uma região do centro-oeste do Brasil. Exame de
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Huang, Yuxiang, and 黃玉祥. "Insights into the molecular basis of the variants: G6PD mahidol and G6PD plymouth." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31243150.

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Chen, Kar-yee Agnes. "Molecular studies of a glucose-6-phosphate dehydrogenase variant /." Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B18156241.

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Books on the topic "G6PD: Glucose-6-Phosphate Dehydrogenase Deficiency"

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Conway, David J. Glucose-6-phosphate dehydrogenase (G6PD) activity as an index of thyroidal stimulation and superoxide metabolism in thyroid cancer. University College Dublin, 1996.

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Parker, James N., and Philip M. Parker. Glucose-6-phosphate dehydrogenase deficiency: A bibliography and dictionary for physicians, patients, and genome researchers [to internet references]. ICON Health Publications, 2007.

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Frequencies of hemoglobin variants: Thalassemia, the glucose-6-phosphate dehydrogenase deficiency, G6PD variants, and ovalocytosis in human populations. Oxford University Press, 1985.

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Wiffen, Philip, Marc Mitchell, Melanie Snelling, and Nicola Stoner. Patient management issues. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199603640.003.0010.

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Drug use in liver disease 178Drug dosing in liver disease 180Hepatorenal syndrome (HRS) 183Drugs in renal impairment 184Drugs in pregnancy 190Drugs in breastfeeding 194Drugs and dietary considerations 198Glucose 6-phosphate dehydrogenase (G6PD) deficiency 200Drugs in porphyria 202Terminology used in liver disease is summarized in ...
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McCann, Shaun R. Red blood cells. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198717607.003.0004.

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Red blood cells, erythrocytes, are unique in that they do not contain a nucleus. This fact facilitates the study of their metabolism. Erythrocytes contain the protein pigment haemoglobin, which is in solution in the cells and consists of globin chains and iron. In this chapter, the development of the understanding of erythrocytes is linked to the blood conditions haemolytic anaemia and paroxysmal nocturnal haemoglobinuria. Premature destruction of erythrocytes, in the absence of blood loss, is termed haemolysis. If the bone marrow is unable to compensate adequately, then anaemia ensues and the
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Red cell disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0002.

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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α thalassaemia
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, Banu Kaya, and Angela Theodoulou. Red cell disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0002_update_001.

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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α‎ thalassaemi
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Livingstone, Frank B. Data on the Abnormal Hemoglobins and Glucose-6-Phosphate Dehydrogenase Deficiency in Human Populations, 1967-1973. University of Michigan, Museum of Anthropology, Publications Department, 2020.

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Carton, James. Haematopathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0015.

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This chapter discusses haematopathology, including iron deficiency anaemia, anaemia of chronic disease, megaloblastic anaemias, hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, thalassaemias, sickle-cell disorders, idiopathic thrombocytopenic purpura (ITP), thrombotic thrombocytopenic purpura (TTP), von Willebrand disease, haemophilia, thrombophilia, acute B-lymphoblastic leukaemia, acute myeloid leukaemias, chronic lymphocytic leukaemia (CLL), chronic myelogenous leukaemia, polycythaemia vera (PV), essential thrombocythaemia (ET), primary myelofibrosis (PMF), myelodyspl
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Wiffen, Philip, Marc Mitchell, Melanie Snelling, and Nicola Stoner. Patient management issues. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198735823.003.0010.

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This chapter outlines information relevant to pharmacists and other healthcare professionals on patient management issues related to special populations. It covers management of patients with liver impairment, including drug use, drug dosing, and hepatorenal syndrome. Drug use and dosing in renal impairment is discussed and the various methods of assessing or calculating glomerular filtration rate are reviewed. The use of drugs in pregnancy and breastfeeding is discussed with guidance given on assessing the risks versus benefits of drug use in these situations. Drugs and dietary considerations
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Book chapters on the topic "G6PD: Glucose-6-Phosphate Dehydrogenase Deficiency"

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Mehlhorn, Heinz. "Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD)." In Encyclopedia of Parasitology. Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_3914.

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Mehlhorn, Heinz. "Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD)." In Encyclopedia of Parasitology. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_3914-1.

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Theisler, Charles. "Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency." In Adjuvant Medical Care. CRC Press, 2022. http://dx.doi.org/10.1201/b22898-155.

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Al Muqati, Hessa Hazza. "Caring for Patients with Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency." In Manual of Pediatric Cardiac Care. Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-5683-8_45.

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Yeung, Chap-Yung. "Erythrocyte glucose-6-phosphate dehydrogenase (G6PD) deficiency and neonatal hyperbilirubinaemia." In Child Health in the Tropics. Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5012-2_27.

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Rickards, O., G. Biondi, G. F. De Stefano, and G. Battistuzzi. "Distribution of Genetically Determined Deficient Variants of Glucose-6-Phosphate Dehydrogenase (G6PD) in Southern Italy." In Advances in Forensic Haemogenetics. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73330-7_115.

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Yaish, Hassan M. "Glucose-6-Phosphate Dehydrogenase Deficiency." In Textbook of Clinical Pediatrics. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_320.

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Chen, Harold. "Glucose-6-Phosphate Dehydrogenase Deficiency." In Atlas of Genetic Diagnosis and Counseling. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6430-3_107-2.

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Qidwai, Tabish. "Glucose 6-Phosphate Dehydrogenase Deficiency." In Exploration of Host Genetic Factors associated with Malaria. Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4761-8_7.

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Timson, David J., Richard J. Reece, James B. Thoden, et al. "Glucose-6-Phosphate Dehydrogenase Deficiency." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_709.

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Conference papers on the topic "G6PD: Glucose-6-Phosphate Dehydrogenase Deficiency"

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Kawulur, Hanna S. I., Hana Krismawati, and Clara Imaniar. "Screening of glucose-6-phosphate dehydrogenase (G6PD) deficiency in two high endemic malaria populations, West Papua province and North Moluccas." In THE 6TH INTERNATIONAL CONFERENCE ON BIOLOGICAL SCIENCE ICBS 2019: “Biodiversity as a Cornerstone for Embracing Future Humanity”. AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0017808.

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Zuchelkowski, B. E., L. Wang, H. F. Penaloza, et al. "Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency of the African American Variant (Val68Met) Protects Against Klebsiella Pneumoniae Intrapulmonary Infection in Mice." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3898.

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Jontari, Hutagalung, Hari Kusnanto, Supargiyono, et al. "A sticky situation: From malaria pre-elimination to gene mutation Glucose-6-Phosphate dehydrogenase deficiency (G6PDd) in Eastern Indonesia." In TOWARDS THE SUSTAINABLE USE OF BIODIVERSITY IN A CHANGING ENVIRONMENT: FROM BASIC TO APPLIED RESEARCH: Proceeding of the 4th International Conference on Biological Science. Author(s), 2016. http://dx.doi.org/10.1063/1.4953501.

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Ahmad, Nermen R., Sayran S. Saleh, and Nihad I. Taha. "Biochemical study for glucose -6-phosphate dehydrogenase (G6PD) in Thalassemia patients." In 2ND INTERNATIONAL CONFERENCE ON APPLIED RESEARCH AND ENGINEERING (ICARAE2022). AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0170649.

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Linsangan, Noel B., Dayne N. Fradejas, Vince Harley D. Gaba, Lester N. Manuel, Jocelyn Flores Villaverde, and Roben A. Juanatas. "Glucose-6-Phosphate Dehydrogenase Deficiency Detection using MyRIO Microcontroller and Color Sensor System." In ICBET 2023: 2023 13th International Conference on Biomedical Engineering and Technology. ACM, 2023. http://dx.doi.org/10.1145/3620679.3620702.

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Wang, Yiping, Lisha Zhou, Yuzheng Zhao, et al. "Abstract 5177: SIRT2 deacetylates and activates glucose-6-phosphate dehydrogenase (G6PD) to protect cells against oxidative stress." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5177.

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Sun, Fengmei, Juan Zhang, and Yuepu Pu. "Glucose-6-phosphate dehydrogenase deficiency and the risk of malaria: A meta-analysis and trial sequential analysis." In 2ND INTERNATIONAL CONFERENCE ON MATERIALS SCIENCE, RESOURCE AND ENVIRONMENTAL ENGINEERING (MSREE 2017). Author(s), 2017. http://dx.doi.org/10.1063/1.5005230.

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Zuchelkowski, B. E., L. Wang, M. Yang, et al. "Evaluation of the Effect of the African Glucose-6-Phosphate Dehydrogenase (G6PD) Polymorphism (Val68Met) on the Acute Inflammatory Response to Endotoxemia in a Humanized Murine Model." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2596.

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Reports on the topic "G6PD: Glucose-6-Phosphate Dehydrogenase Deficiency"

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หลุยเจริญ ชีพสุนทร, ชาลิสา, та พูลลาภ ชีพสุนทร. ผลของภาวะพร่องเอนไซม์ G6PD ต่อการเสื่อมของเซลล์ไตในโรคเบาหวาน. คณะแพทยศาสตร์ จุฬาลงกรณ์มหาวิทยาลัย, 2018. https://doi.org/10.58837/chula.res.2018.30.

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เอนไซม์ glucose 6-phosphate dehydrogenase (G6PD) เป็นเอนไซม์ที่พบได้ในทุกเซลล์ของร่างกาย มีหน้าที่สร้าง nicotinamide adenine dinucleotide (NADPH) จากวิถี pentose phosphate pathway (PPP) เพื่อช่วยป้องกันภาวะ oxidative stress ภายในเซลล์ด้วยการรักษาระดับ reduced glutathione (GSH) ความผิดปกติที่เกิดขึ้นกับเอนไซม์ G6PD ส่งผลกระทบต่อเซลล์จากภาวะ oxidative stress เช่น ภาวะพร่องเอนไซม์ G6PD สามารถเหนี่ยวนำให้เซลล์ไตเกิด apoptosis และ nephropathy นอกจากนี้ยังพบภาวะพร่องเอนไซม์ G6PD เพิ่มสูงขึ้นในผู้ป่วยเบาหวานเมื่อเทียบกับคนปกติ ด้วยเหตุนี้จึงเป็นที่มาของการศึกษาวิจัยบทบาทของภาวะพร่องเอนไซม์ G6PD ในเซล
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