- Neonatal Health and Biochemistry
- Erythrocyte Function and Pathophysiology
- Metabolism and Genetic Disorders
- Polish Historical and Cultural Studies
- Lymphoma Diagnosis and Treatment
- Chronic Lymphocytic Leukemia Research
- Hemoglobinopathies and Related Disorders
- Heme Oxygenase-1 and Carbon Monoxide
- Immune Cell Function and Interaction
- Theology and Canon Law Studies
- Central European Literary Studies
- High Altitude and Hypoxia
- Methemoglobinemia and Tumor Lysis Syndrome
- Hemoglobin structure and function
- T-cell and Retrovirus Studies
- Cancer, Hypoxia, and Metabolism
- Historical and Archaeological Studies
- Language and Culture
- Metabolomics and Mass Spectrometry Studies
- Folate and B Vitamins Research
- Cytomegalovirus and herpesvirus research
- Acute Lymphoblastic Leukemia research
- Historical and Cultural Studies of Poland
- Childhood Cancer Survivors' Quality of Life
- T-cell and B-cell Immunology
University of Virginia
2019-2024
University of Colorado Anschutz Medical Campus
2023
Carter Center
2022
University of Virginia Cancer Center
2019-2021
The Red blood cell (RBC) storage lesion results in decreased circulation and function of transfused RBCs. Elevated oxidant stress impaired energy metabolism are a hallmark the both human murine Although studies don't suffer concerns that findings may not translate, they do from genetic environmental variability amongst subjects. Murine models can control for genetics, environment, much interventional experimentation be carried out mice is neither technically feasible nor ethical humans....
Abstract Background Increases in the red blood cell (RBC) degree of fatty acid desaturation are reported response to exercise, aging, or diseases associated with systemic oxidant stress. However, no studies have focused on presence and activity desaturases (FADS) mature RBC. Study design methods Steady state metabolomics isotope‐labeled tracing experiments, immunofluorescence approaches, pharmacological interventions were used determine unsaturation, FADS as a function storage, stress, G6PD...
The red blood cell (RBC)-Omics study, part of the larger NHLBI-funded Recipient Epidemiology and Donor Evaluation Study (REDS-III), aims to understand genetic contribution donor RBC characteristics. Previous work identified demographic, behavioral, genetic, metabolic underpinnings donation, storage, (to a lesser extent) transfusion outcomes, but none have yet linked bodies work. We performed genome-wide association (GWA) analysis using RBC-Omics study participants with generated untargeted...
Deficiency of glucose-6-phosphate dehydrogenase (G6PD) is the single most common enzymopathy, present in approximately 400 million humans (approximately 5%). Its prevalence hypothesized to be due conferring resistance malaria. However, G6PD deficiency also results hemolytic sequelae from oxidant stress. Moreover, associated with kidney disease, diabetes, pulmonary hypertension, immunological defects, and neurodegenerative diseases. To date, only available mouse models have decreased levels...
Glucose 6-phosphate dehydrogenase (G6PD) deficiency is the most common enzymopathy in humans (∼5% of all individuals). G6PD (G6PDd) caused by an unstable enzyme and manifests strongly red blood cells (RBCs) that cannot synthesize new protein. G6PDd RBCs have decreased ability to mitigate oxidative stress due lower levels NADPH, as a result defective pentose phosphate pathway. Accordingly, drugs can hemolysis potentially life-threatening anemia patients. Dapsone highly useful drug for...
Primaquine and tafenoquine are the only approved drugs that can achieve a radical cure for <i>Plasmodium vivax</i> malaria but contraindicated in patients who deficient glucose 6-phosphate dehydrogenase (G6PDd) due to risk of severe hemolysis from reactive oxygen species (ROS) generated by redox cycling drug metabolites. 5-hydroxyprimaquine its quinone-imine cause robust red blood cells (RBCs), so labile as not be detected or urine. Rather, 5,8-quinoneimine is rapidly converted into...
Glucose-6-phosphate dehydrogenase (G6PD) deficiency affects 500 million people globally, impacting red blood cell (RBC) antioxidant pathways and increasing susceptibility to hemolysis under oxidative stress. Despite the systemic generation of reactive oxygen species during exercise, effects exercise on individuals with G6PD remain poorly understood This study utilized humanized mouse models expressing Mediterranean variant (S188F, 10% enzymatic activity) investigate performance molecular...
The murine CMV (MCMV) immunoevasin m04/gp34 escorts MHC class I (MHC I) molecules to the surface of infected cells where these complexes bind Ly49 inhibitory receptors (IRs) and prevent NK cell attack. Nonetheless, certain self-MHC I-binding activating are able promote robust expansion antiviral immunity during MCMV infection. A basis for I-dependent sensing MCMV-infected targets control infection however remains unclear. In this study, we discovered that Ly49R activation receptor is...
Abstract The Red Blood Cell (RBC)-Omics study, part of the larger NHLBI-funded Recipient Epidemiology and Donor Evaluation Study (REDS-III), aims to understand genetic contribution blood donor RBC characteristics. Previous work identified demographic, behavioral, metabolic underpinnings donation, storage, - a lesser extent transfusion outcomes, but none have yet linked bodies work. We performed Genome-Wide Association (GWA) analysis using RBC-Omics study participants with generated...
Glucose-6-phosphate-dehydrogenase deficiency (G6PD) is the most common enzymatic in humans, affecting ~500 million people, ~6% of mankind. G6PD rate limiting enzyme pentose phosphate pathway and controls generation NADPH. NADPH an essential reducing equivalent for primary antioxidant pathways humans that associated with protection against onset intra- extra-vascular hemolysis response to oxidant stress. While stress known elicit mild moderate physiological deficiency, information limited...
Abstract Deficiency of Glucose 6 phosphate dehydrogenase (G6PD) is the single most common enzymopathy, present in approximately 400 million humans (e.g. 5% humans). Its prevalence hypothesized to be due conferring resistance malaria. However, G6PD deficiency also results hemolytic sequelae from oxidant stress. Moreover, associated with kidney disease, diabetes, pulmonary hypertension, immunological defects, and neurodegenerative diseases. To date, only available mouse models have decreased...