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https://www.readbyqxmd.com/read/28103504/l-arginine-alters-the-effect-of-5-fluorouracil-on-breast-cancer-cells-in-favor-of-apoptosis
#1
Mozhgan Jahani, Mehri Azadbakht, Fatemeh Norooznezhad, Kamran Mansouri
Chemoresistance in breast cancer is a major obstacle, especially in p53 mutation types. The aim of this study was to evaluate if a combination therapy of l-arginine with 5-fluorouracil (5-FU) can alter the effect of this chemotherapy drug on breast cancer cells. The study was performed on BT-20 and MCF-7 cell lines. The effects of l-arginine alone and in combination with 5-FU were investigated on cell viability, apoptosis and nitric oxide (NO) production. Drugs effects on the cellular energetic metabolism were investigated through the lactate production and glucose-6-phosphate dehydrogenase (G6PD) activity assay...
January 16, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28099116/determination-of-glucose-6-phosphate-dehydrogenase-cut-off-values-in-a-tunisian-population
#2
Naouel Laouini, Chaima Abdelhafidh Sahli, Latifa Jouini, Sabrine Haloui, Sondes Hadj Fredj, Rym Daboubi, Hajer Siala, Faida Ouali, Meriam Becher, Nourelhouda Toumi, Amina Bibi, Taieb Messsaoud
BACKGROUND: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the commonest enzymopathy worldwide. The incidence depends essentially on the methods used for the assessment. In this respect, we attempted in this study to set cut-off values of G6PD activity to discriminate among normal, heterozygous, and deficient individuals using the World Health Organization (WHO) classification and the receiver operating characteristics (ROC) curve analysis. METHODS: Blood samples from 250 female and 302 male subjects were enrolled in this study...
January 18, 2017: Clinical Chemistry and Laboratory Medicine: CCLM
https://www.readbyqxmd.com/read/28097104/massive-hemolysis-causing-renal-failure-in-acute-hepatitis-e-infection
#3
Pragya Karki, Sarthak Malik, Bipadabhanjan Mallick, Vishal Sharma, Surinder S Rana
Acute viral hepatitis is usually a self-limiting illness. However, it can lead to complications that can be life-threatening, such as acute liver failure. Glucose 6 phosphate dehydrogenase (G6PD) deficiency in the setting of acute viral hepatitis can lead to a massive hemolysis, manifesting as acute kidney injury and markedly raised bilirubin levels; although cases are rare. Here, we report such a case. The patient had a viral hepatitis E infection and presented with kidney injury requiring dialysis. Examination showed very high mixed hyperbilirubinemia due to massive intravascular hemolysis...
December 28, 2016: Journal of Clinical and Translational Hepatology
https://www.readbyqxmd.com/read/28096627/altered-oxidative-stress-and-carbohydrate-metabolism-in-canine-mammary-tumors
#4
K Jayasri, K Padmaja, M Saibaba
AIM: Mammary tumors are the most prevalent type of neoplasms in canines. Even though cancer induced metabolic alterations are well established, the clinical data describing the metabolic profiles of animal tumors is not available. Hence, our present investigation was carried out with the aim of studying changes in carbohydrate metabolism along with the level of oxidative stress in canine mammary tumors. MATERIALS AND METHODS: Fresh mammary tumor tissues along with the adjacent healthy tissues were collected from the college surgical ward...
December 2016: Veterinary World
https://www.readbyqxmd.com/read/28092180/n-acetylcysteine-a-possible-protector-against-indomethacin-induced-peptic-ulcer-crosstalk-between-antioxidant-anti-inflammatory-and-antiapoptotic-mechanisms
#5
Nema Ali Soliman, Doaa Hussein Zineldeen, Mohamed Alaa Katary, Darin Abd Ali
This study investigated the gastroprotective effects of N-acetylcysteine (NAC) against indomethacin-induced gastric ulcer in rats. Ulceration was induced by a single oral administration of indomethacin (30 mg/kg). 50 male albino rats were allocated into 5 equal groups: control group received normal saline orally, indomethacin group rats received normal saline orally for 5 days and indomethacin (50 mg/kg) on the last day, ranitidine group received ranitidine (reference drug) orally for 5 days (50 mg/kg) before receiving indomethacin (50 mg/kg) on the last day, and NAC groups received NAC orally at 300 and 500 mg/kg, respectively, for 5 days before receiving indomethacin (50 mg/kg) on the last day...
November 14, 2016: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/28090457/glucose-6-phosphate-dehydrogenase-deficiency-does-not-increase-the-susceptibility-of-sperm-to-oxidative-stress-induced-by-h2o2
#6
Shiva Roshankhah, Zahra Rostami-Far, Farhad Shaveisi-Zadeh, Abolfazl Movafagh, Mitra Bakhtiari, Jila Shaveisi-Zadeh
OBJECTIVE: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme defect. G6PD plays a key role in the pentose phosphate pathway, which is a major source of nicotinamide adenine dinucleotide phosphate (NADPH). NADPH provides the reducing equivalents for oxidation-reduction reductions involved in protecting against the toxicity of reactive oxygen species such as H2O2. We hypothesized that G6PD deficiency may reduce the amount of NADPH in sperms, thereby inhibiting the detoxification of H2O2, which could potentially affect their motility and viability, resulting in an increased susceptibility to infertility...
December 2016: Clinical and Experimental Reproductive Medicine
https://www.readbyqxmd.com/read/28079896/impaired-embryonic-development-in-glucose-6-phosphate-dehydrogenase-deficient-caenorhabditis-elegans-due-to-abnormal-redox-homeostasis-induced-activation-of-calcium-independent-phospholipase-and-alteration-of-glycerophospholipid-metabolism
#7
Tzu-Ling Chen, Hung-Chi Yang, Cheng-Yu Hung, Meng-Hsin Ou, Yi-Yun Pan, Mei-Ling Cheng, Arnold Stern, Szecheng J Lo, Daniel Tsun-Yee Chiu
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a commonly pervasive inherited disease in many parts of the world. The complete lack of G6PD activity in a mouse model causes embryonic lethality. The G6PD-deficient Caenorhabditis elegans model also shows embryonic death as indicated by a severe hatching defect. Although increased oxidative stress has been implicated in both cases as the underlying cause, the exact mechanism has not been clearly delineated. In this study with C. elegans, membrane-associated defects, including enhanced permeability, defective polarity and cytokinesis, were found in G6PD-deficient embryos...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28078984/rasburicase-induced-methemoglobinemia-in-a-patient-with-glucose-6-phosphate-dehydrogenase-deficiency
#8
Maliha Khan, Shilpa Paul, Saad Farooq, Thein Hlaing Oo, Priya Ramshesh, Nitin Jain
BACKGROUND: Rasburicase is commonly used in patients with hematologic malignancies for tumor lysis syndrome prophylaxis and management. Methemoglobinemia is a serious rare adverse effect of rasburicase, more common in patients with G6PD deficiency. Prompt diagnosis and appropriate management of this condition can make the difference between successful recovery and significant morbidity. Here we discuss the link of rasburicase with methemoglobinemia and the pathophysiology behind increased incidence of this side effect in G6PD deficient patients...
January 11, 2017: Current Drug Safety
https://www.readbyqxmd.com/read/28078493/false-positive-newborn-screen-using-the-beutler-spot-assay-for-galactosemia-in-glucose-6-phosphate-dehydrogenase-deficiency
#9
Grace Stuhrman, Stefanie J Perez Juanazo, Kea Crivelly, Jennifer Smith, Hans Andersson, Eva Morava
Classical galactosemia is detected through newborn screening by measuring galactose-1-phosphate uridylyltransferase (GALT) in the USA primarily via the Beutler spot assay. We report on an 18-month-old patient with glucose-6-phosphate dehydrogenase (G6PD) deficiency that was originally diagnosed with classical galactosemia. The patient presented with elevated liver function enzymes and bilirubinemia and was immediately treated with soy-based formula. Confirmatory tests revealed deficiency of the GALT enzyme, however, full-sequencing of GALT was normal, suggestive of a different ideology...
January 12, 2017: JIMD Reports
https://www.readbyqxmd.com/read/28069791/prolonged-indirect-hyperbilirubinemia-in-a-moderately-preterm-boy-with-mediterranean-glucose-6-phosphate-dehydrogenase-and-glutathione-s-transferase-mu-1-null-mutations
#10
Sameer Yaseen Al-Abdi
A 33-week gestation boy with Mediterranean glucose-6-phosphate dehydrogenase (G6PD) and a glutathione S-transferase Mu 1 null mutations (GSTM1*0/*0) developed prolonged indirect hyperbilirubinemia (PIH). He had no laboratory evidence of haemolysis or infection, and no exposure to oxidising agents. He has two full-term older brothers who have no history of neonatal hyperbilirubinemia. One brother, who was exclusively breast fed, has only Mediterranean G6PD and the other has only GSTM1*0/*0. The three boys have no mutation in the uridine diphosphate glucuronosyltransferase 1A1 gene...
January 9, 2017: BMJ Case Reports
https://www.readbyqxmd.com/read/28067620/characterisation-of-the-opposing-effects-of-g6pd-deficiency-on-cerebral-malaria-and-severe-malarial-anaemia
#11
Geraldine M Clarke, Kirk Rockett, Katja Kivinen, Christina Hubbart, Anna E Jeffreys, Kate Rowlands, Muminatou Jallow, David J Conway, Kalifa A Bojang, Margaret Pinder, Stanley Usen, Fatoumatta Sisay-Joof, Giorgio Sirugo, Ousmane Toure, Mahamadou A Thera, Salimata Konate, Sibiry Sissoko, Amadou Niangaly, Belco Poudiougou, Valentina D Mangano, Edith C Bougouma, Sodiomon B Sirima, David Modiano, Lucas N Amenga-Etego, Anita Ghansah, Kwadwo A Koram, Michael D Wilson, Anthony Enimil, Jennifer Evans, Olukemi K Amodu, Subulade Olaniyan, Tobias Apinjoh, Regina Mugri, Andre Ndi, Carolyne M Ndila, Sophie Uyoga, Alexander Macharia, Norbert Peshu, Thomas N Williams, Alphaxard Manjurano, Nuno Sepúlveda, Taane G Clark, Eleanor Riley, Chris Drakeley, Hugh Reyburn, Vysaul Nyirongo, David Kachala, Malcolm Molyneux, Sarah J Dunstan, Nguyen Hoan Phu, Nguyen Ngoc Quyen, Cao Quang Thai, Tran Tinh Hien, Laurens Manning, Moses Laman, Peter Siba, Harin Karunajeewa, Steve Allen, Angela Allen, Timothy Me Davis, Pascal Michon, Ivo Mueller, Síle F Molloy, Susana Campino, Angeliki Kerasidou, Victoria J Cornelius, Lee Hart, Shivang S Shah, Gavin Band, Chris Ca Spencer, Tsiri Agbenyega, Eric Achidi, Ogobara K Doumbo, Jeremy Farrar, Kevin Marsh, Terrie Taylor, Dominic P Kwiatkowski
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is believed to confer protection against Plasmodium falciparum malaria, but the precise nature of the protective effecthas proved difficult to define as G6PD deficiency has multiple allelic variants with different effects in males and females, and it has heterogeneous effects on the clinical outcome of P. falciparum infection. Here we report an analysis of multiple allelic forms of G6PD deficiency in a large multi-centre case-control study of severe malaria, using the WHO classification of G6PD mutations to estimate each individual's level of enzyme activity from their genotype...
January 9, 2017: ELife
https://www.readbyqxmd.com/read/28062797/targeted-proteomics-for-multiplexed-verification-of-markers-of-colorectal-tumorigenesis
#12
Anuli Christiana Uzozie, Nathalie Selevsek, Asa Wahlander, Paolo Nanni, Jonas Grossmann, Achim Weber, Federico Buffoli, Giancarlo Marra
Targeted proteomic methods can accelerate the verification of multiple tumor marker candidates in large series of patient samples. We utilized the targeted approach known as selected / multiple reaction monitoring (SRM/MRM) to verify potential protein markers of colorectal adenoma identified by our group in previous transcriptomic and quantitative shotgun proteomic studies of a large cohort of precancerous colorectal lesions. We developed SRM assays to reproducibly detect and quantify 25 (62.5%) of the 40 selected proteins in an independent series of precancerous and cancerous tissue samples (19 adenoma/normal mucosa pairs; 17 adenocarcinoma/normal mucosa pairs)...
January 4, 2017: Molecular & Cellular Proteomics: MCP
https://www.readbyqxmd.com/read/28059001/possible-association-of-3-utr-357-a-g-ivs11-nt-93-t-c-c-1311-c-t-polymorphism-with-g6pd-deficiency
#13
Mahmoud M Sirdah, Mohammad E Shubair, Mustafa S Al-Kahlout, Jamal M Al-Tayeb, Josef T Prchal, N Scott Reading
BACKGROUND: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common X-linked inherited enzymopathic disorder affecting more than 500 million people worldwide. It has so far been linked to 217 distinct genetic variants in the exons and exon-intron boundaries of the G6PD gene, giving rise to a wide range of biochemical heterogeneity and clinical manifestations. OBJECTIVES: Reports from different settings suggested the association of intronic and other mutations outside the reading frame of the G6PD gene with reduced enzyme activity and presenting clinical symptoms...
January 6, 2017: Hematology (Amsterdam, Netherlands)
https://www.readbyqxmd.com/read/28041936/the-regulation-of-the-pentose-phosphate-pathway-remember-krebs
#14
REVIEW
Juan Ignacio Ramos-Martinez
The changes in gene expression and posttranslational modifications of enzymes are comprised in the concept of "coarse control" of the oxidative phase of the pentose phosphate pathway. However, these changes are slow in its implementation. The defensive mechanism against oxidative stress requires a most rapid response, impossible to achieve with coarse regulation systems. Recently, it has been suggested that a quick acceleration mechanism of G6PD activity could be produced by the reduction of NADPH-inhibition of G6PD...
January 15, 2017: Archives of Biochemistry and Biophysics
https://www.readbyqxmd.com/read/28034875/plasma-cell-leukemia-revealing-a-g6pd-deficiency
#15
Anna Raimbault, Nicolas Chapuis
No abstract text is available yet for this article.
December 29, 2016: Blood
https://www.readbyqxmd.com/read/28028996/genetic-profiles-of-korean-patients-with-glucose-6-phosphate-dehydrogenase-deficiency
#16
Jaewoong Lee, Joonhong Park, Hayoung Choi, Jiyeon Kim, Ahlm Kwon, Woori Jang, Hyojin Chae, Myungshin Kim, Yonggoo Kim, Jae Wook Lee, Nack Gyun Chung, Bin Cho
BACKGROUND: We describe the genetic profiles of Korean patients with glucose-6-phosphate dehydrogenase (G6PD) deficiencies and the effects of G6PD mutations on protein stability and enzyme activity on the basis of in silico analysis. METHODS: In parallel with a genetic analysis, the pathogenicity of G6PD mutations detected in Korean patients was predicted in silico. The simulated effects of G6PD mutations were compared to the WHO classes based on G6PD enzyme activity...
March 2017: Annals of Laboratory Medicine
https://www.readbyqxmd.com/read/28002512/pharmacotoxicological-screening-on-new-derivatives-of-beta-phenylethylamine-potential-agonists-of-beta3-adrenergic-receptors
#17
Simona Negreş, Anca Zanfirescu, Floriana Elvira Ionică, Elena Moroşan, Bruno Ştefan Velescu, Oana Cristina Şeremet, Cristina Elena Zbârcea, Emil Ştefănescu, Manuella Militaru, Andreea LetiŢia Arsene, Denisa Marilena Margină, Livia Uncu, Corina Scutari, Cornel ChiriŢă
BACKGROUND AND AIMS: Beta3-adrenergic receptors (beta3-ARs) have been initially characterized in 1989. Afterwards, their tissue distribution was established: white and brown adipose tissue, central nervous system, myocardium (atrial and ventricular), blood vessels, smooth gastrointestinal muscles (stomach, small intestine, colon), gallbladder, urinary bladder, prostate, skeletal muscles. Non-clinical trials have demonstrated the major implication of beta3-ARs in glucose metabolism, implicitly, in insulin release, and also in obesity...
2016: Romanian Journal of Morphology and Embryology, Revue Roumaine de Morphologie et Embryologie
https://www.readbyqxmd.com/read/27981932/g6pd-deficiency-with-arnold-chiari-malformation
#18
Shilpi Verma, Pradeep Kumar Bhatia, Vandana Sharma, Priyanka Sethi, Yogendra Raj Singh
A neonate with glucose-6-phosphate dehydrogenase (G6PD) deficiency and Arnold-Chiari Malformation (ACM) type 2 underwent lumbar meningomyelocele (MMC) repair. Patients with G6PD deficiency are prone to develop haemolysis following any kind of oxidative stress and in ACM, there is a disturbed cranio-spinal pressure relationship. The neonate was managed under general anaesthesia with propofol for induction as well as for maintenance along with fentanyl and oxygen-nitrous mixture.
November 2016: Journal of the College of Physicians and Surgeons—Pakistan: JCPSP
https://www.readbyqxmd.com/read/27980749/glucose-6-phosphate-dehydrogenase-deficiency-not-exclusively-in-males
#19
Leonie van den Broek, Evelien Heylen, Machiel van den Akker
Glucose-6-phosphate (G6PD) deficiency is the most common human enzyme defect, often presenting with neonatal jaundice and/or acute hemolytic anemia, triggered by oxidizing agents. G6PD deficiency is an X-linked, hereditary disease, mainly affecting men, but should also be considered in females with an oxidative hemolysis.
December 2016: Clinical Case Reports
https://www.readbyqxmd.com/read/27976504/a-novel-flow-cytometry-based-method-of-analyzing-heinz-bodies
#20
D Palasuwan, A Palasuwan, A Charoensappakit, E Noulsri
INTRODUCTION: Heinz bodies are important to diagnosing and managing patients. However, microscopic examination of Heinz bodies has several disadvantages, demonstrating the need for a better method. We explored the potential use of flow cytometry to examine Heinz bodies. METHODS: Whole-blood samples were collected from patients deficient in G6PD and healthy volunteers. Acetylphenylhydrazine was used to induce formation of Heinz bodies in red blood cells (RBCs). Then, RBCs positive for Heinz bodies were examined using a FACSCanto II cytometer...
December 15, 2016: International Journal of Laboratory Hematology
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