A5007351184- Neonatal Health and Biochemistry
- Catalysts for Methane Reforming
- Asymmetric Synthesis and Catalysis
- Erythrocyte Function and Pathophysiology
- Catalytic Processes in Materials Science
- Synthetic Organic Chemistry Methods
- Methemoglobinemia and Tumor Lysis Syndrome
- Chemical Safety and Risk Management
- Organic Chemistry Cycloaddition Reactions
- Oxidative Organic Chemistry Reactions
- Congenital Diaphragmatic Hernia Studies
- Catalysis for Biomass Conversion
- Chemistry and Chemical Engineering
- Catalysis and Oxidation Reactions
- Various Chemistry Research Topics
- Hemoglobin structure and function
- Hyperglycemia and glycemic control in critically ill and hospitalized patients
- Metabolism and Genetic Disorders
Stanford University
2015-2021
Washington State University
2019-2020
Laguna College of Art and Design
2013
Glucose-6-phosphate dehydrogenase (G6PD) deficiency, one of the most common human genetic enzymopathies, is caused by over 160 different point mutations and contributes to severity many acute chronic diseases associated with oxidative stress, including hemolytic anemia bilirubin-induced neurological damage particularly in newborns. As no medications are available treat G6PD here we seek identify a small molecule that corrects it. Crystallographic study mutagenesis analysis structural...
We study the hydrogenation of CO under ambient pressure conditions over a Co-MnOx model catalyst using chemical transient kinetics (CTK) calibrated molecular flow conditions. Alkanes and alkenes are shown to form with markedly differing kinetics. Quantitation data allows accumulating carbon oxygen coverages be determined at any instant "buildup" transients. Anderson–Schulz–Flory (ASF) chain lengthening probabilities evaluated while approaching steady-state reaction. A linear dependence these...
Significance Mechanism of the loss activity most severe patient-derived mutants glucose-6-phosphate dehydrogenase (G6PD) deficiency has remained elusive despite availability G6PD structures for decades. Structural and biophysical investigations have revealed a common mechanism dynamics how these mutations hinder substrate-binding site, reducing enzymatic activity. These are triggered by long-distance propagation structural defects at dimer interface binding site noncatalytic cofactor....
New reactions and reagents that allow for multiple bond-forming events per synthetic operation are required to achieve structural complexity thus value with step-, time-, cost-, waste-economy. Here we report a new class of function like tetramethyleneethane (TME), allowing back-to-back [4 + 2] cycloadditions, thereby amplifying the complexity-increasing benefits Diels–Alder metal-catalyzed cycloadditions. The parent recursive reagent, 2,3-dimethylene-4-trimethylsilylbutan-1-ol (DMTB), is...
Abstract We recently identified AG1, a small‐molecule activator that functions by promoting oligomerization of glucose‐6‐phosphate dehydrogenase (G6PD) to the catalytically competent forms. Biochemical experiments indicate activation G6PD original hit molecule (AG1) is noncovalent and one C 2 ‐symmetric region homodimer important for ligand function. Consequently, disulfide in AG1 not required G6PD, number analogues were prepared without this reactive moiety. Our study supports mechanism...
A chemical research program at a public high school has been developed. The full-year Advanced Chemical Research class (ACR) in the enrolls 20–30 seniors each year, engaging them long-term experimental projects. Through partnerships involving university scientists, ACR students have had opportunity to explore number of highly sophisticated original As an example quality work made possible through these school–university partnerships, this article describes development novel method for...
A one-pot procedure is developed consisting of a Diels—Alder reaction the tetramethyleneethane equivalent (II) and dienophiles, subsequent elimination to give second diene, captured in [4 + 2] cycloaddition afford compounds like (IV).
Oxidative stress caused by infection, medication, food, and imbalance of metabolic cycles damages DNA organelles, which may lead to cancer, blood disorders, other serious diseases. Glucose‐6‐phosphate dehydrogenase (G6PD) is the rate‐limiting enzyme in pentose phosphate pathway, essential for nucleotide, fatty acid, cholesterol, hormone synthesis. In addition those roles, G6PD reduces NADP + NADPH, crucial reducing reactive oxygen species. Dysfunction increases susceptibility oxidative...