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Dissertations / Theses on the topic 'G6PD: Glucose-6-Phosphate Dehydrogenase Deficiency'

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Published: 7 June 2025

Last updated: 2 August 2025

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1

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

陳嘉儀 and Kar-yee Agnes Chen. "Molecular studies of a glucose-6-phosphate dehydrogenase variant." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31212906.

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12

區詠娥 and Wing-ngor Au. "Expression and three dimensional (3-D) X-ray structure of human glucose-6-phosphate dehydrogenase (G6PD) variants." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31236509.

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Au, Wing-ngor. "Expression and three dimensional (3-D) X-ray structure of human glucose-6-phosphate dehydrogenase (G6PD) variants /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B18865550.

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14

Kwok, Colin, and 郭浩然. "A study of the quaternary structure of human glucose-6-phosphate dehydrogenase (G6PD)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31245468.

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15

Talukdar, Indrani. "Signaling pathways involved in regulation of glucose-6-phosphate dehydrogenase (G6PD) by arachidonic acid." Morgantown, W. Va. : [West Virginia University Libraries], 2006. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4673.

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Thesis (Ph. D.)--West Virginia University, 2006.<br>Title from document title page. Document formatted into pages; contains viii, 123 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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16

Ganczakowski, Mary Elizabeth. "Thalassaemia, glucose-6-phosphate dehydrogenase deficiency and malaria in Vanatu, S.W. Pacific." Thesis, University of London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420824.

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17

Griffith, Brian Nelson. "The study of glucose-6-phosphate dehydrogenase (G6PD) gene regulation in HepG2 cells by glucose induction and the study of G6PD mRNA localization by fluorescent in situ hybridization (FISH)." Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2511.

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Thesis (M.S.)--West Virginia University, 2002.<br>Title from document title page. Document formatted into pages; contains viii, 100 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 80-96).

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18

Nkhoma, Ella T. Meshnick Steven R. "Malaria and pregnancy outcomes in an area of high HIV and glucose-6-phosphate dehydrogenase deficiency prevalence." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2009. http://dc.lib.unc.edu/u?/etd,2846.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2009.<br>Title from electronic title page (viewed Jun. 4, 2010). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Epidemiology, Gillings School of Global Public Health." Discipline: Epidemiology; Department/School: Public Health.

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19

Shah, Shivang Satish. "Examining the relationship between genetic variation at G6PD and severe malaria." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:933063af-9cd9-4f74-94c9-55ef2db28551.

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Glucose-6-phosphate dehydrogenase (G6PD) deficiency, a common heritable trait whose prevalence mirrors geographic patterns of historic malaria endemicity, is thought to confer a selective advantage owing to partial protection conferred against malaria. Direct evidence supporting this malaria protection hypothesis in the form of clinical association studies remains controversial, however, as conflicting results have been reported with respect to the strength and specificity of a protective effect, if any, conferred to carriers of G6PD deficiency-associated alleles. This thesis examines genetic

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20

Marques, Cálita Pollyanna. "Padronização da análise dos produtos da PCR/RFLP que amplifica os genes Ribossomal Internal transcribed spacer (ITS) e Glucose-6- phosphate dehydrogenase (G6PD) para identificação de Leishmania spp. em gel de poliacrilamida." Universidade Federal de Goiás, 2017. http://repositorio.bc.ufg.br/tede/handle/tede/7789.

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Submitted by Franciele Moreira (francielemoreyra@gmail.com) on 2017-09-21T20:25:51Z No. of bitstreams: 2 Dissertação - Cálita Pollyanna Marques - 2017.pdf: 1468493 bytes, checksum: 90300902d8a48fc5600761dfccf90324 (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5)<br>Approved for entry into archive by Luciana Ferreira (lucgeral@gmail.com) on 2017-09-22T11:43:21Z (GMT) No. of bitstreams: 2 Dissertação - Cálita Pollyanna Marques - 2017.pdf: 1468493 bytes, checksum: 90300902d8a48fc5600761dfccf90324 (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (M

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21

Liu, You Cheng, and 劉祐丞. "Altered Caenorhabditis elegans Phenotypes by Double Deficiency of Glucose-6-Phosphate Dehydrogenase (G6PD) and Isocitrate Dehydrogenase 1 (IDH-1)." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/9jfpkf.

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碩士<br>長庚大學<br>醫學生物技術暨檢驗學系<br>104<br>Glucose-6-phosphate dehydrogenase (G6PD) is the rate-limiting enzyme of pentose phosphate pathway. It produces nicotinamide adenine dinucleotide phosphate (NADPH) and ribose, which are necessary for many cellular activities. G6PD knockout mice results in embryonic death, yet the mechanism of which remains unclear. Our previous report has show that G6PD-deficient Caenorhabditis elegans (C. elegans), established by ribonucleic acid interference (RNAi), produces defective embryos. Intriguingly, parental G6PD-deficient C. elegans shows no apparent growth defect.

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22

Lin, Min-Shuan, and 林旻萱. "Molecular Mechanism Underlines UV-A Irradiation Induced Apoptosis in Normal and Glucose-6-phosphate Dehydrogenase(G6PD) –deficient Human Skin Fibroblasts: A Confocal Microscopic Study." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/15477803844119691015.

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碩士<br>高雄醫學大學<br>生物醫學檢驗學研究所<br>96<br>Glucose-6-phosphate dehydrogenase (G6PD) is involved in the generation of NADPH for the proper maintenance of the cellular redox balance. G6PD deficiency predispose human fibroblasts (HFF) to retarded growth and accelerated cellular senescence. In addition, human dermal fibroblasts are subjected to deeply penetrating UVA irradiation. The effects of UVA on cell components of normal fibroblasts have been documented to result from a photodynamic action producing reactive oxygen species (ROS) that can indirectly affect different cellular targets. However, the de

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23

AN, WU LI, and 吳禮安. "Role of Reactive Oxygen Species (ROS) and Mitochondria Calcium Overloading on the Folic Acid Deprivation-Triggered Apoptosis of Glucose-6-Phosphate Dehydrogenase (G6PD)-Deficient Human Foreskin Fibroblasts." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/51443919650091922411.

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碩士<br>長庚大學<br>醫學生物技術研究所<br>94<br>Glucose-6-phosphate dehydrogenase (G6PD) is involved in the generation of NADPH for the proper maintenance of the cellular redox balance, G6PD deficiency predispose human fibroblasts (HFF) to retarded growth and accelerated cellular senescence. Thus far, the pivotal role of a micronutrient, such as folic acid, on the cellular functions of the normal and G6PD-deficient HFF have never been investigated. The objectives of the present research are two-fold: (1) To explore the possibility that folic acid deficiency can trigger the occurrence of apoptotic cell dea

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24

Ho, Hung-yao, and 何鴻耀. "1. Oxidative stress and senescence: a model based on the study of the glucose-6-phosphate dehydrogenase (G6PD)-deficient cells. 2. The role of MEKK in T cell activation." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/76039822958303829052.

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博士<br>國防醫學院<br>生命科學研究所<br>88<br>英文摘要 The first part of the thesis is concerned with the effect of glucose-6-phosphate dehydrogenase (G6PD) deficiency on the physiology of nucleated cells. Glucose-6-phosphate dehydrogenase (G6PD) is involved in the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) and the maintenance of the cellular redox balance. Biological effects of G6PD were studied using G6PD-deficient human foreskin fibroblasts (HFF). Cell growth parameters, namely, the growth rate and cell cycle profile, were examined in a primary G6PD-deficient cell st

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25

Zakaria, Nurul Aili. "Studies of glucose-6-phosphate dehydrogenase." Phd thesis, 2016. http://hdl.handle.net/1885/117368.

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Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme that catalyzes the conversion of glucose-6-phosphate to 6-phosphoglucolactone with the reduction of NADP+ to NADPH. It is the first component of the pentose phosphate pathway (PPP) that is a central and important biochemical pathway. The PPP functions to produce building block compounds and intermediates for energy production. The first three enzymes of the PPP are referred to as the oxidative phase and produce NADPH that is crucial for dealing with oxygen stress, especially in people with G6PD defici

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26

Dangerfield, Bruce. "The characterisation of glucose-6-phosphate dehydrogenase (G6PD) variation in the malagasy." Thesis, 1997. https://hdl.handle.net/10539/23740.

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Much of the history of the peoples of Madagascar, the Malagasy, is unknown and uncertain. The human inhabitants of Madagascar show a large amount of biological diversity. Studies of physical appearance, linguistics, ethnology, archaeology and history have implicated the African, Indonesian, Arabian, Indian and Chinese populations in contributing to the present-day diversity of the people of Madagascar. The major contributors to the inhabitants of Madagascar appear to be the African and Indonesian populations. Large amounts of African admixture are said to be present in the lowland ethnic group

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27

Chen, Hua-Ling, and 陳華玲. "Biochemical characterization of new glucose-6-phosphate dehydrogenase (G6PD) mutations and analysis of the dimerization domain of G6PD protein." Thesis, 2001. http://ndltd.ncl.edu.tw/handle/93566013399575380357.

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博士<br>國立臺灣大學<br>動物學研究所<br>89<br>Glucose-6-phosphate dehydrogenase (G6PD; EC 1.1.1.49) is a housekeeping enzyme that catalyzes the first and rate-limiting step in the pentose phosphate pathway (PPP). It oxidizes glucose-6-phosphate to 6-phosphogluconolactone, reducing NADP+ to NADPH. The major physiological role of G6PD in mature red blood cells is to produce NADPH, which is required for a number of reductive biosynthesis and for detoxification of hydrogen peroxide and other compound. G6PD deficiency is the most common human enzymopathy affecting over 400 million people worldwide. The clinical

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28

"Pro-oxidative effect of Chinese herbal medicine on glucose-6-phosphate dehydrogenase deficiency." Thesis, 2006. http://library.cuhk.edu.hk/record=b6074271.

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For the development of a G6PD-deficient mouse model, we introduced the mutant Gpdxa-m1Neu allele (a severe ENU-induced mutation that results in 13-15% G6PD activities of wild type littermates) into the C57L/J background (a strain that constitutively exhibits low G6PD activity) through a breeding program. Of significance is that 78% of the F2 generation had G6PD activities <2 U/g Hb, levels similar to those of severe G6PD deficiency in human. The efficacy of this model was preliminary verified by the known haemolytic agent, naphthalene, as demonstrated by the decrease of GSH/GSSG ratio by 24

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Shao-Mei and 黃少玫. "Influence of Glucose-6-Phosphate Dehydrogenase Deficiency in Zebrafish Embryos During Early Development." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/62977532007383482878.

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碩士<br>中山醫學大學<br>醫學檢驗暨生物技術學系碩士班<br>98<br>The Glucose-6-phosphate dehydrogenase (G6PD) is the housekeeping enzyme in pentose phosphate pathway, which the nicotinamide adenine dinucleotide phosphates (NADPH) is generated as intracellular reduction potentials to overcome the oxidative stresses in cells. To date, not much have been done to reveal the role of this important metabolic enzyme in early embryo development. In this study, we take the advantage of using zebrafish as an animal model to explore the role of G6PD in early embryo development. Through G6PD-morpholino (G6PD-MO) injecting, the G6

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30

Hsu, Wan-Lin, and 徐宛琳. "Investigating interaction networks for drug-induced glucose-6-phosphate dehydrogenase deficiency-related hemolysis." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/38082545986976855470.

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碩士<br>高雄醫學大學<br>藥學系碩士在職專班<br>104<br>Glucose 6-phosphate dehydrogenase deficiency, an X-linked disorder, is the most common enzymatic disorder of red blood cells in humans. It can cause hemolysis after exposure to drugs with a high redox potential, fava beans, selected infections, or metabolic abnormalities. Several drugs have been found to be high risk of hemolytic anemia for G6PD deficiency patients. However, there is no standard method to evaluate drugs for their risks of hemolytic anemia. We propose to utilize ChemDIS system to study the interaction network of drugs and proteins and identif

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31

Wu, Hsin-Fang, and 吳昕芳. "Mining structural and physicochemical features for drug-induced glucose-6-phosphate dehydrogenase deficiency-related hemolysis." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/9ukrky.

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碩士<br>高雄醫學大學<br>藥學系碩士在職專班<br>103<br>The pentose phosphate pathway is an important metabolic pathway in red blood cells involved in the oxidation of glucose. The deficiency of Glucose-6-Phosphate Dehydrogenase (G6PD), an essential enzyme in the pentose phosphate pathway, can result in abnormal metabolism. Patients with G6PD deficiency, an X-linked recessive genetic condition, can not contact or take camphor, Vicia faba and sulfa drugs, because it may cause hemolytic anemia. There is a considerable higher prevalence in Taiwan from a newborn screening program for G6PD deficiency, especially for t

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32

Jia-Yu, Lin, and 林家瑜. "Study of the expression pattern of human glucose-6-phosphate dehydrogenase (G6PD) in human cancer cell lines and the effects of anticancer drugs in G6PD-overexpressing fibroblast cells." Thesis, 1999. http://ndltd.ncl.edu.tw/handle/00649096569800693760.

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碩士<br>國立臺灣大學<br>動物學研究所<br>87<br>G6PD (glucose-6-phosphate dehydrogenase) catalyzes the convert of G6P(glucose-6-phosphate) to 6PG(6-phsphgluconate) which is accompanied with the formation of NADPH in the first step of pentose phoshate pathway (PPP). In this manner, the PPP provides the major source of pentoses in the cells for DNA and RNA synthesis. The cellular level of NADPH is closely relative to the activation of catalase and the synthesis of GSH (glutathione). Previous reports indicated that the activity of G6PD was proportional to the growth rate of normal cells and high G6PD activities

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Chiang, Whei-Ling, and 江蕙玲. "The Aberrant Expression of Carbonic Anhydrase Isoenzyme in Glucose-6-phosphate Dehydrogenase Deficiency and Non-small Cell Lung Cancer in Taiwan." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/32394113357926889702.

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博士<br>中山醫學大學<br>生物化學研究所<br>92<br>Part I: Glucose-6-phosphate dehydrase (G6PD) deficiency, an X-linked abnormality, is caused by one of a multitude of allelic G6PD variants with reduced enzyme activity. This defect is usually well tolerated, except for acute haemolytic crises associated with an oxidative stress, such as drugs, fava beans ingestion, and infection. The concentration of carbonic anhydrase (CA) has been demonstrated to be elevated in several types of anemia. This study was designed to evaluate the alternations in quantities and activities of cytosolic CA isoenzymes and

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