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This technology includes a method of correcting the motion during T1 mapping using cardiovascular magnetic resonance imaging (MRI). Ischemic heart disease is the leading cause of death in the United States. The lack of blood supply among myocardial tissue, especially for scar regions, changes the T1 relaxation value of heart muscles. The non-invasive quantification of T1 value of myocardium (T1 mapping) is therefore of great importance for the diagnosis and treatment of cardiovascular disease.

This technology includes mechanobiological nucleic acid nanoassemblies-based platforms with dynamically controlled efficiency of T-cell activation. T-cells are the central players in adaptive immune response led by a T-cell receptor (TCR) centric machinery. Current T-cell activation strategy (e.g., micron-scale beads) focuses on 2D TCR-agonist biomimetic surfaces and biomimetic 2D immune synapses with planar traction, which requires non-physiological hyper-stimulatory cytokines levels (e.g., IL-2), and thus, is incompatible with clinical applications.

This technology includes a novel capsid protein for recombinant adeno-associated virus (AAV)-mediated gene transfer evaluation. We have identified a "fossilized" endogenous AAV sequence element (referred to as mAAV-EVE) within the germline of an ancient lineage of Australian marsupials and have cloned and sequenced mAAV-EVE orthologs from at least fifteen lineage-specific taxa.

This technology includes efficient lentiviral gene delivery system for both guide RNA and Cas9 endonuclease as a method to cure sickle cell disease. Gene correction is an ideal gene therapy strategy for hereditary disease, including sickle cell disease.

This technology includes in vitro-generated trophectoderm (TE) cells, which are ideal for modeling diseases of the placenta, drug screening, and cell-based therapies. The TE lineage which gives rise to placental cells during early human development. Derivation of definitive placental cells from human pluripotent stem cells in culture remains controversial and so far, placental cells can only be derived directly from primary placental tissue, which largely limits their access and study in the laboratory.

This technology includes a novel cardiac patch which was 3D printed to repair damaged cardiac tissue. Based on biological and anatomical understanding of myocardial tissue, a novel 3D bioprinting technique was developed to directly fabricate the cellularized and vascularized cardiac patch with anisotropic fiber and perfusable vessel architecture. The design will integrate biomimetic aligned myocardial fibers and perfusable blood vessels to create a thick, functional cardiac patch, suitable for the human heart implantation.

This technology includes the use of nanodiamonds to achieve background-free imaging. We present several techniques to reduce or eliminate background florescence by exploiting properties of the fluorescent nanodiamonds. In particular, magnetic field modulation of the fluorescence intensity offers a simple, robust, and easily adaptable method to obtain background free imaging in a variety of imaging modalities, i.e., fluorescence microscopy and wide field fluorescence animal imaging.

This technology includes the use of LZK and DLK inhibitors to be used for the treatment of head and neck squamous cell carcinoma (HNSCC) or lung squamous cell carcinoma (LSCC). Specifically, we demonstrate that inhibitors that can be repurposed to target LZK suppresses LZK kinase-dependent stabilization of MYC and activation of the PI3K/AKT pathway. In vivo preclinical cell line xenograft mouse model demonstrates that targeting LZK will suppress tumor growth. We also demonstrate that several additional compounds potently inhibit LZK and could serve as new therapeutic modalities.

This technology includes Spodoptera frugiperda (Sf9) cells which were developed to produce recombinant adeno-associated virus. The cells maintain a copy of the vector genome and for production, require infection with a single baculovirus that expresses either structural and nonstructural proteins to produce rAAV, or the non-structural (Rep) proteins to produce ceDNA.

The technology described involves the use of a compound called prazole as an anti-viral agent specifically targeting HIV-1. It was found that prazole binds to a protein called Tsg101, which is crucial for the virus's life cycle. This binding disrupts the normal interaction of Tsg101 with another protein, ubiquitin, thereby inhibiting the release of HIV-1 particles from infected cells. Additionally, the interference caused by prazole leads to the degradation of the viral protein Gag within host cells.