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glucose 6 phosphate dehydrogenase/sembap
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ABO incompatibility and glucose-6-phosphate dehydrogenase deficiency presenting as Hydrops Foetalis.
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ABO incompatibility and glucose-6-phosphate dehydrogenase deficiency G6PD are common haematological problems affecting the newborn. The resulting haemolytic disease of foetus and newborn (HDFN) caused by either of these pathologies generally follows a benign course. It is typically characterized by
Bilateral pulmonary edema after endoscopic sympathectomy in a patient with glucose-6-phosphate dehydrogenase deficiency.
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Transaxillary endoscopic sympathectomy of thoracic ganglia (T2-T3) has recently gained wider acceptance as the treatment of choice for palmar hyperhidrosis. It requires one-lung ventilation to facilitate the surgery. One-lung ventilation, however, is not without complications, among which acute
Hydrops fetalis and stillbirth in a male glucose-6-phosphate dehydrogenase-deficient fetus possibly due to maternal ingestion of sulfisoxazole; a case report.
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A model of glucose-6-phosphate dehydrogenase deficiency in the zebrafish.
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Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common genetic defect and enzymopathy worldwide, affecting approximately 400 million people and causing acute hemolysis in persons exposed to prooxidant compounds such as menthol, naphthalene, antimalarial drugs, and fava beans. Mouse
Recurrent idiopathic nonimmune hydrops fetalis: A case report.
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A recurrent idiopathic nonimmune hydrops fetalis case in two subsequent pregnancies was observed in a woman with no child. In both pregnancies, all the detailed analysis, including a high level of ultrasonography, amniocentesis, serologic evaluation, routine blood work, hemoglobin electrophoresis,
Inhibition of rabbit lung glucose-6-phosphate dehydrogenase by dehydroepiandrosterone augments oxidant injury.
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The contribution of lung glucose-6-phosphate dehydrogenase (G-6-PD) activity to pulmonary antioxidant defenses was investigated in the isolated perfused rabbit lung using dehydroepiandrosterone (DHEA), a specific steroidal inhibitor of G-6-PD. Infusion of xanthine oxidase (0.002 U/ml) generated
Protection with cycloheximide or emetine against pulmonary edema induced by ozone or nitrogen dioxide.
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Pretreatment with cycloheximide or emetine provided significant protection against pulmonary edema in rats exposed to ozone or nitrogen dioxide. Other inhibitors of protein-synthesis, actinomycin D or puromycin, failed to show such effects. Possible actions of these agents as well as the doses and
[Hydrops fetalis and G-6-PD deficiency].
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BACKGROUND
Antenatal manifestation of glucose-6-phosphate dehydrogenase deficiency is uncommon.
METHODS
A male was born by caesarian section at 34 weeks of GA for hydrops fetalis (HF). Fetal ultrasonography showed hydrops fetalis for the first time at 24 weeks of GA. All investigations were normal,
Human platelets modulate edema formation in isolated rabbit lungs.
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The role of platelet glucose-6-phosphate dehydrogenase (G-6-PD) in mediating the effects of human platelets on oxidant-induced edema in the isolated perfused rabbit lung was investigated using dehydroepiandrosterone, a specific steroidal inhibitor of G-6-PD. Xanthine oxidase (0.003 and 0.012 U/ml)
Patterns of sickle cell, thalassaemia and glucose-6-phosphate dehydrogenase deficiency genes in north-western Saudi Arabia.
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This study was conducted on 429 blood samples collected from Saudi males and females from Al-Ula in the north-western province of Saudi Arabia in order to determine the frequency of the sickle cell gene, glucose-6-phosphate dehydrogenase (G6PD) deficiency gene, and alpha- and beta-thalassaemia
Hematologic disorders and nonimmune hydrops fetalis.
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Hematologic disorders are implicated in approximately 10% to 27% of cases of nonimmune hydrops fetalis. In almost all of these disorders, anemia leading to heart failure, edema, ascites, and anasarca is the final common denominator. The etiology of the anemia in these cases can be conveniently
Nonimmune hydrops fetalis caused by G6PD deficiency hemolytic crisis and congenital dyserythropoietic anemia.
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We present a case of a female neonate who had a nonimmune hydrops fetalis and severe hemolytic anemia due to a rare combination of glucose-6-phosphate dehydrogenase (G6PD) deficiency and congenital dyserythropoietic anemia. We conclude that in severe cases with persistent anemia one should search
The ocular findings in glucose-6-phosphate dehydrogenase deficiency.
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57 cases with G6PD deficiency and 62 with normal G6PD activities as controls in Chonghua County, Guangdong Province were examined in the respects of visual acuity, color vision, corneal sensitivity, lens, vitreous and fundus. The results showed that the incidences of congenital lenticular opacities
S-allyl L-cysteine diminishes cerebral ischemia-induced mitochondrial dysfunctions in hippocampus.
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Ischemic brain is highly vulnerable to free radicals mediated secondary neuronal damage especially mitochondrial dysfunctions. Present study investigated the neuroprotective effect of S-allyl L-cysteine (SAC), a water soluble compound from garlic, against cerebral ischemia/reperfusion (I/R)-induced
Effects of desipramine on the antioxidant status in rat tissues at carrageenan-induced paw inflammation.
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The pathogenesis of many diseases and different pathological conditions, including inflammation, is associated with excess production of reactive oxygen species (ROS). The present study aimed to investigate the effects of the antidepressant desipramine (DES) on carrageenan (CG)-induced inflammation,
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