A product and method of using albumin nanoparticles for treating multiple traumas by augmenting the function or effectiveness of stem cells or precursor cells in vivo. An albumin nanoparticle suspension containing submicron albumin spheres is prepared, with the albumin spheres being capable of augmenting a function and effectiveness of stem cells or precursor cells in vivo for treating multiple traumas at the same time. A predetermined amount of the albumin nanoparticle suspension is administered to a patient before or after an onset of multiple traumas. A function of the stem or precursor cells can be augmented or improved by the albumin spheres to stimulate mobilization toward the traumas, to ameliorate an inflammatory response of the subject by decreasing an amount of RANTES endothelial production on cytokines production, and/or to improve a secretion of fractalkine. The albumin spheres can be bound with fibrinogen molecules in vitro or in vivo.

A method of treating or preventing adverse outcomes associated with tissue plasminogen activator (tPA) administration, cerebral edema-related side effects, cerebral edema associated with radiation therapy, or migraine headaches by administering an effective amount of a SUR1-TRPM4 channel inhibitor, such as glyburide, and optionally the co-administration of a second therapeutically active agent, to a subject in need thereof. Adverse outcomes associated with tPA include cerebral hemorrhage, cerebral edema, physical impairment or death. The administration of the SUR1-TRPM4 channel inhibitors occurs prior to the radiation therapy, during the radiation therapy, after the radiation therapy, or combinations thereof. The SUR1-TRPM4 channel inhibitor is administered prior to surgical excision of a brain tumor, CAR-T therapy, or administration of flutarabine. Alternatively, or in addition, the SUR1-TRPM4 channel inhibitor is administered prior the onset of the cerebral edema-related side effects.

Disclosed herein is an agent that modulates a cis interaction between Repulsive Guidance Molecule A (RGMa) and Neogenin or lipid rafts. Modulation by the agent may include blocking the cis interaction between RGMa and Neogenin and/or disrupting lipid rafts. In turn, this promotes neuronal cell survival and axon growth and/or regeneration. Also disclosed herein is a method of treating a disease in a subject in need thereof. The method may include administering the agent to the subject. Further disclosed herein is a method of identifying an agent that modulates the cis interaction between RGMa and Neogenin.

The present invention relates to the technical field of bio-pharmaceuticals, and in particular relates to use of prourokinase and its variants against coagulopathy caused by viruses. It has been found that use of prophylactic doses of prourokinase or its variants in virus-infected patients can effectively prevent formation of thrombus and clots without increasing the risk of bleeding, thereby effectively preventing coagulopathy, such as disseminated intravascular coagulation, ST-segment elevation myocardial infarction, ischemic stroke, pulmonary embolism, deep veins thrombosis, and venous thromboembolism caused by viruses. When virus infection causes thrombosis in a patient, a thrombolytic therapy with a therapeutic dose of prourokinase or its variants can effectively dissolve the thrombus and lower the risk of death and disability. The present invention fully demonstrates in terms of both prophylaxis and treatment that when viral infection causes coagulopathy, prourokinase and its variants can reduce the damage and possible sequelae caused by the virus to patients, and improve survival of the patients.

Provided herein are deuterated RUC-4 compounds, and related compositions and therapeutic methods.

Biomarkers useful for the diagnosis and treatment of acute ischemic stroke are disclosed. Also provided is a quantitative assay method for accurately identifying transcript number in a biological sample.

The disclosure relates to compositions and methods of treating, improving, and accelerating the healing of large segmental bone defects in a subject. The method comprises administering to a patient in need of treatment an effective amount of whole blood, sodium citrate, ecarin and BMP-2.

The present invention is directed to methods of treatment of airway obstruction associated with fibrin-containing cast formation by administering a fibrinolytic agent.

The technology described herein is directed methods of treating an extracellular vesicle (EV)-associated disease or vascular calcification in subject by administration of an agent that reduces the levels or activity of Annexin A1 (ANXA1).

The present disclosure provides, at least in part, methods and compositions for in vivo fusosome delivery. In some embodiments, the fusosome comprises a combination of elements that promote specificity for target cells, e.g., one or more of a fusogen, a positive target cell-specific regulatory element, and a non-target cell-specific regulatory element. In some embodiments, the fusosome comprises one or more modifications that decrease an immune response against the fusosome.