Molecular Detection and Viral-Load Quantification for HIV-1 Groups M, N and O, and Simian Immunodeficiency Virus-cpz (SIVcpz)

This invention provides materials, methods, and assays for detecting HIV-1 groups M and O and optionally HIV-1 group N and simian immunodeficiency virus-cpz (SIV-cpz). Specific nucleic acid primers for hybridization, amplification, and detection of HIV-1 are also provided for. The nucleic acid amplification assays can detect small concentrations of HIV-1 and are also useful for quantitative examinations of viral load concentrations within biological samples.

Simple, Rapid, and Sensitive Real-Time PCR Assays for Detecting Drug Resistance of HIV

This novel assay features real-time PCR reagents and methods for detecting drug-resistance related mutations in HIV, for newly diagnosed patients and those individuals currently receiving antiretroviral therapies. As the use of antiretroviral compounds to treat HIV infection proliferates, viruses adapt and evolve mutations limiting the efficacy of these drugs and disrupting the success of treatment.

Multiplexing Homocysteine in Primary Newborn Screening Assays Using Maleimides as Select Derivatization Agents

Homocystinuria (HCU), a group of inherited disorders, causes symptoms ranging from failure to thrive and developmental delays in infants or young children to abnormal blood clots with onset in adults.1 Approximately 1 in 200,000 to 335,000 people have HCU globally.2

An Automated System for Myocardial Perfusion Mapping and Machine Diagnosis to Detect Ischemic Heart Disease with First-pass Perfusion Cardiac Magnetic Resonance Imaging

This technology includes a fully automated computer aided diagnosis system to quantify myocardial blood flow (MBF) and myocardial perfusion reserve (MPR) pixel maps from the first-pass contrast-enhanced cardiac magnetic resonance (CMR) perfusion images. This system performs automated image registration, motion compensation, segmentation, and modeling to extract quantitative features from different myocardial regions of interest.

Next-Generation 5-HT-2B Serotonin-Receptor Antagonists for Anti-Fibrotic & Cardiopulmonary Therapy

This technology includes a family of small-molecule antagonists that selectively block the 5-HT2B serotonin receptor—an upstream driver of tissue-remodeling—to address fibrotic, cardiopulmonary and related disorders. Built on a conformationally-locked “(N)-methanocarba” nucleoside scaffold, the compounds show nanomolar potency, >30–400-fold selectivity over the closely related 5-HT2C receptor, and favorable oral bioavailability in rodents.

Improved PE-based Targeted Toxins: A Therapeutic with Increased Effectiveness

Targeted toxins (e.g., immunotoxins) are therapeutics that have at least two important components: (1) a toxin domain that is capable of killing cells and (2) a targeting domain that is capable of selectively localizing the toxic domain to only those cells which should be killed. By selecting a targeting domain that binds only to certain diseased cells (e.g., a cell which only expresses a cell surface receptor when in a diseased state), targeted toxins can kill the diseased cells while allowing healthy, essential cells to survive.

System for Automated Anatomical Structures Segmentation of Contrast-Enhanced Cardiac Computed Tomography Images

This technology includes a fully automatic 3D image processing system to segment the heart as well as other organs from contrast-enhanced cardiac computed tomography (CCT) images. Our method detects four cardiac chambers including left ventricle, right ventricle, left atrium, right atrium, as well as the ascending aorta and left ventricular myocardium. It also classifies noncardiac tissue structures in the CCT images such as lung, chest wall, spine, descending aorta, and liver.

First in class Small Molecule Agonists of the mammalian Relaxin family receptor 1 (RXFP1) and use in treatment of cancer, fibrotic, and vascular disorders (HHS Ref No. E-145-2024-0-US-02)

It is well documented in literature that activation of RXFP1 by relaxin induces: 1) up-regulation of the endothelin system which leads to vasodilation; 2) extracellular matrix remodeling through regulation of collagen deposition, cell invasiveness, proliferation, and overall tissue homeostasis; 3) a moderation of inflammation by reducing levels of inflammatory cytokines, such as TNF-a and TGF-b; and 4) angiogenesis by activating transcription of VEGF.

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