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Production of inflammatory molecules in peripheral blood mononuclear cells from severely glucose-6-phosphate dehydrogenase-deficient subjects.

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OBJECTIVE We have previously demonstrated that Mediterranean glucose-6-phosphate dehydrogenase (G6PD)-deficient peripheral blood mononuclear cells (PBMC) respond to mitogenic stimuli with a reduced cholesterol synthesis and growth. In the present study, we have investigated the release of

Increase in glucose-6-phosphate dehydrogenase in adipocytes stimulates oxidative stress and inflammatory signals.

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In adipocytes, oxidative stress and chronic inflammation are closely associated with metabolic disorders, including insulin resistance, obesity, cardiovascular disease, and type 2 diabetes. However, the molecular mechanisms underlying these metabolic disorders have not been thoroughly elucidated. In

Irreversible inhibition of glucose-6-phosphate dehydrogenase by the coenzyme A conjugate of ketoprofen: a key to oxidative stress induced by non-steroidal anti-inflammatory drugs?

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Oxidative damage by non-steroidal anti-inflammatory drugs (NSAIDs) has been considered relevant to the occurrence of gastro-intestinal side-effects. In the case of chiral arylpropionate derivatives like ketoprofen (KPF), this mechanism has been evidenced for the R-enantiomer, especially when chiral

Age, Ethnicity, Glucose-6-Phosphate Dehydrogenase Deficiency, Micronutrient Powder Intake, and Biomarkers of Micronutrient Status, Infection, and Inflammation Are Associated with Anemia Among Children 6-59 Months in Nepal.

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Anemia is a major concern for children in Nepal; however, little is known about context-specific causes of anemia.We used cross-sectional data from the 2016 Nepal National Micronutrient Status Survey to evaluate factors associated with anemia in a

Glucose-6-phosphate dehydrogenase deficiency and the inflammatory response to endotoxin and polymicrobial sepsis.

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OBJECTIVE Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common human genetic polymorphism. The deficiency protects against malaria but was shown to worsen the clinical course after severe trauma. This study tested whether the deficiency is associated with altered cytokine responses in

Glucose-6-Phosphate Dehydrogenase Deficiency Improves Insulin Resistance With Reduced Adipose Tissue Inflammation in Obesity.

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Glucose-6-phosphate dehydrogenase (G6PD), a rate-limiting enzyme of the pentose phosphate pathway, plays important roles in redox regulation and de novo lipogenesis. It was recently demonstrated that aberrant upregulation of G6PD in obese adipose tissue mediates insulin resistance as a result of

The role of glucose-6-phosphate dehydrogenase in adipose tissue inflammation in obesity.

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Obesity is closely associated with metabolic diseases including type 2 diabetes. One hallmark characteristics of obesity is chronic inflammation that is coordinately controlled by complex signaling networks in adipose tissues. Compelling evidence indicates that reactive oxygen species (ROS) and its

20-HETE-induced mitochondrial superoxide production and inflammatory phenotype in vascular smooth muscle is prevented by glucose-6-phosphate dehydrogenase inhibition.

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20-Hydroxyeicosatetraeonic acid (20-HETE) produced by cytochrome P-450 monooxygenases in NADPH-dependent manner is proinflammatory, and it contributes to the pathogenesis of systemic and pulmonary hypertension. In this study, we tested the hypothesis that inhibition of glucose-6-phosphate

[Glucose-6-phosphate dehydrogenase activity in patients with chronic inflammatory lung diseases].

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The activity of the key enzyme of the pentoso-phosphate cycle--glucoso-6-phosphatedehydrogenase was examined in patients with chronic inflammatory pulmonary diseases. Results indicate that with exacerbation of the process in the bronchopulmonary system there occurs an increase of the activity of the

Safe neoadjuvant trastuzumab-based treatment in HER2 + inflammatory early breast cancer in a glucose 6-phosphate dehydrogenase-deficient postmenopausal woman: A case report and review of the literature.

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Glucose 6-phosphate dehydrogenase (G6PD) is a basic antioxidant pathway for erythrocytes, being its deficiency the most common gene mutation worldwide. As breast cancer is one of the most frequent tumors, many of these patients may present with G6PD deficiency prior treatment without

[Use of the NSAID ketoprofen lysine salt in glucose-6-phosphate dehydrogenase (G6PD) deficiency in inflammatory disease in children].

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Nineteen young females, aged 4 months-13 years, suffering from intermediate erythrocyte G6PD deficiency plus 14 hemizygote males, aged 6 months and 16 years, and one dizigote and completely deficient female were treated with ketoprofen lysine salt for upper and lower respiratory tract diseases. The

[Variations in sorbitol dehydrogenase, 6-phospho-gluconate dehydrogenase, and glucose 6-phosphate dehydrogenase activities in the adrenal glands of the rabbit after ingestion of non-steroid anti-inflammatory drugs].

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Severe inflammatory reaction following corneal collagen cross-linking in a patient with glucose-6-phosphate dehydrogenase deficiency.

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Oxidative stress, inflammation and carcinogenesis are controlled through the pentose phosphate pathway by transaldolase.

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Metabolism of glucose through the pentose phosphate pathway (PPP) influences the development of diverse pathologies. Hemolytic anemia due to deficiency of PPP enzyme glucose 6-phosphate dehydrogenase is the most common genetic disease in humans. Recently, inactivation of another PPP enzyme,

In vivo effects of curcumin on the paraoxonase, carbonic anhydrase, glucose-6-phosphate dehydrogenase and β-glucosidase enzyme activities in dextran sulphate sodium-induced ulcerative colitis mice.

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Increases in the risk of infections and malignancy due to immune suppressive therapies of inflammatory bowel diseases (IBDs) have led the researchers to focus on more nontoxic and acceptable natural products like curcumin. Here we investigate whether prophylactic and therapeutic application of the

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