Browse Technologies

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Vanderbilt researchers have developed a method to perform the Parahydrogen Induced Polarization (PHIP) based method of Signal Amplification by Reversible Exchange (SABRE) in aqueous media. This allows the resulting hyperpolarized molecules to be used for in vivo applications.

Vanderbilt researchers have developed heterogeneous catalysis and catalyst for the NMR Signal Amplification by Reversible Exchange (SABRE) hyperpolarization process. Coupled with the researchers' development of a method to perform SABRE in aqueous solutions, this discovery could allow fully biocompatible SABRE hyperpolarization processes in water with catalyst recycling. This would allow the production of pure aqueous contrast agents requiring only parahydrogen as a consumable.

Inventors at Vanderbilt University have developed a novel chemical design and synthesis process for azulene-based COX2 contrast agents which can be used for molecular imaging, via a variety of imaging techniques. These COX2 probes can be utilized for numerous applications, including imaging cancers and inflammation caused by arthritis and cardiovascular diseases. The process for developing these COX2 contrast agents has been significantly improved through a convergent synthesis process which reduces the required steps to establish the COX2 precursors.

Vascular inflammation caused by metabolic, autoimmune, and microbial insults mediates cardiovascular diseases that include hypertension and atherosclerosis (heart attacks, strokes), systemic lupus, and giant cell arteritis. An estimated 35 million Americans have hypercholesterolemia, contributing to 500,000 deaths underlying heart attacks and strokes. In these diseases, metabolic, autoimmune, and microbial insults continually challenge blood and vascular cells by triggering signaling to the nucleus mediated by BCL10. Genetic ablation of BCL10 rescues animals from atherosclerosis, aortic aneurysms, and fatty liver and insulin resistance due to overnutrition. Intracellular therapy with CP-CRADD is designed to extinguish BCL10-mediated noxious signals to avert vascular inflammation and its life-threatening complications including ruptured aneurysms in aorta and brain.