211 G to A variation of UGT1A1 and severe neonatal hyperbilirubinemia
We read with great interest the article by Yang et al.1 that reported that UGT1A1 variation, Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency, and thalassemia may contribute to severe neonatal hyperbilirubinemia in southern China. Although this is an interesting and important finding that may have clinical implications, this study has some limi tations, and we would like to make some comments on this article.
Neutrophils are the most abundant, short lived, and terminally differentiated leukocytes with distinct tiers of arsenals to counter pathogens. Neutrophils were traditionally considered transcriptionally inactive cells, but recent researches in the field led to a paradigm shift in neutrophil biology and revealed subpopulation heterogeneity, and functions pivotal to immunity and inflammation. Furthermore, recent unfolding of metabolic plasticity in neutrophils has challenged the long-standing concept of their sole dependence on glycolytic pathway. Metabolic adaptations and distinct regulations have been identified which are ...
Publication date: Available online 18 September 2019Source: Redox BiologyAuthor(s): Margaret M. Loniewska, Anmol Gupta, Shama Bhatia, Isabel MacKay-Clackett, Zhengping Jia, Peter G. WellsAbstractMice deficient in glucose-6-phosphate dehydrogenase (G6PD) cannot replenish the cellular antioxidant glutathione, which detoxifies neurodegenerative reactive oxygen species (ROS). To determine the functional consequences of G6PD deficiency, young and aging G6PD-deficient mice were evaluated for brain G6PD activity, DNA damage (comets, γH2AX), Purkinje cell loss, brain function (electrophysiology, behaviour) and lifespan. DNA ...
Conditions: G6PD Deficiency; Stroke Interventions: Drug: Aspirin; Drug: Clopidogrel Sponsor: First Affiliated Hospital, Sun Yat-Sen University Not yet recruiting
Condition: G6PD Deficiency Intervention: Drug: Sodium Chromate Cr51 Sponsors: Columbia University; New York Blood Center Completed