Curative and prophylactic therapies for microvascular and/or macrovascular thrombosis are provided, as are prophylactic therapies capable of preventing fibrinolysis shutdown and therapies for non-thrombotic disorders. Methods provide for administering a therapeutically effective amount of an annexin A2.

Curative and prophylactic therapies for microvascular and/or macrovascular thrombosis are provided, as are prophylactic therapies capable of preventing fibrinolysis shutdown and therapies for non-thrombotic disorders. Methods provide for administering a therapeutically effective amount of an annexin A2.

Provided herein are methods of enhancing mechanical thrombectomy during endovascular therapy for acute thrombosis using 3,3′-diindolylmethane.

The present disclosure provides use of icaritin in preparing a drug for preventing and treating a bleeding disorder and belongs to the field of medicine. The icaritin can relieve platelet dysfunction, shorten thromboplastin time, and promote blood coagulation, and can be used for preventing and treating the bleeding disorder, especially for treating hemorrhagic transformation after cerebral infarction, gastrointestinal bleeding caused by a thrombolytic or antithrombotic drug for cerebral infarction, or a bleeding complication of a thrombolytic or antithrombotic drug for myocardial infarction.

Provided is a gene for trypsin-like serine protease, a protein encoded thereby and use thereof. The nucleotide sequence of the gene for trypsin-like serine protease is set forth in SEQ ID No. 1, the amino acid sequence of the protein encoded by the gene for trypsin-like serine protease is set forth in SEQ ID No. 2. The protein encoded by the gene provided by the present disclosure is capable of inhibiting P. aeruginosa, A. hydrophila, V. parahaemolyticus and V. harveyi.

The present invention relates to plasminogen for use in a method for treating or preventing lung dysfunction associated with the formation of hyaline membranes in a patient, wherein the patient is preferably further administered with at least one plasminogen activator.

The invention includes pharmaceutical compositions that diminish and/or dissolve calcium deposits in arterial walls, methods for diminishing and/or dissolving calcium deposits in arterial walls, and methods for making and administering such compositions. The compositions comprise oral dosage forms of serrapeptase, nattokinase, vitamin D3 and vitamin K2 administered twice daily.

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

Compositions and methods are provided for the cell-mediated targeted killing of diseased cells based on the presence of an intracellular antigen, rather than a surface-bound marker. The targeting cells are modified to express a cytotoxic protein that is delivered into a targeted cell, and after delivery is selectively activated by the presence of a cytoplasmic protein of interest. In one embodiment of the invention, the cytotoxic molecule is a Granzyme B (GrB) polypeptide. In the compositions of the invention, GrB is modified to render its cytotoxic enzymatic functions inactive, until the presence of an intracellular antigen unlocks the GrB molecule to enable enzymatic activities.

The present invention provides methods and combinations for reducing the infarct volume in a tissue of a subject undergoing ischemia or at risk of developing ischemia.