In one aspect, the invention provides a peptide comprising a chaperone-mediated autophagy (CMA)-targeting signal domain; a protein-binding domain that selectively binds to a target cytosolic protein; and a cell membrane penetrating domain (CMPD). In another aspect, the invention provides methods for reducing the intracellular expression level of an endogenous target protein in vitro and in an animal, wherein the method involves administration of the peptide. Methods are also provided for treating a pathological condition in an animal, the methods comprising administering the peptide to the animal. In one embodiment, the pathological condition is a neurodegenerative disease. In another embodiment of the invention, the target cytosolic protein is death associated protein kinase 1 and the CMPD is protein transduction domain of the HIV-1 Tat protein.

The invention relates to a method for prognosing ACS in a subject, the method comprising determining plasma MIF and Nt-proBNP (or BNP) concentrations in a sample from the subject, diagnosing ACS when the subject plasma concentrations are greater than a reference MIF and Nt-proBNP (or BNP) plasma concentration, and prognosing the magnitude of ACS from the subject plasma MIF and Nt-proBNP (or BNP) concentrations. Also provided is a method of treating ACS in a subject, a device, a kit, and a cardiac biomarker related to the methods of prognosing ACS.

The invention relates to a method for prognosing ACS in a subject, the method comprising determining plasma MIF and Nt-proBNP (or BNP) concentrations in a sample from the subject, diagnosing ACS when the subject plasma concentrations are greater than a reference MIF and Nt-proBNP (or BNP) plasma concentration, and prognosing the magnitude of ACS from the subject plasma MIF and Nt-proBNP (or BNP) concentrations. Also provided is a method of treating ACS in a subject, a device, a kit, and a cardiac biomarker related to the methods of prognosing ACS.

Treatment of subjects experiencing cerebral ischemia is improved when the treatment employs a thrombolytic and an inhibitor against vascular endothelial growth factor receptor signal transduction (VEGF-RST) at a reduced, low dosage compared to that used to treat cancer patients. The treatment is also improved to permit point-of-care use by formulating protein drugs for long term stability at room temperature, providing doses appropriate for the method, and by combining the therapeutic agents with a point-of-care diagnostic for blood brain barrier integrity.

Treatment of subjects experiencing cerebral ischemia is improved when the treatment employs a thrombolytic and an inhibitor against vascular endothelial growth factor receptor signal transduction (VEGF-RST) at a reduced, low dosage compared to that used to treat cancer patients. The treatment is also improved to permit point-of-care use by formulating protein drugs for long term stability at room temperature, providing doses appropriate for the method, and by combining the therapeutic agents with a point-of-care diagnostic for blood brain barrier integrity.

A method is disclosed to dissolve protein deposited in muscle. The method includes the step of administering an effective amount of an agent selected from the group consisting of fibrinolytics, proteolytics, photolytic and magnelytic agents.

Treatment of subjects experiencing cerebral ischemia is improved when the treatment employs a thrombolytic and an inhibitor against vascular endothelial growth factor receptor signal transduction (VEGF-RST) at a reduced, low dosage compared to that used to treat cancer patients. The treatment is also improved to permit point-of-care use by formulating protein drugs for long term stability at room temperature, providing doses appropriate for the method, and by combining the therapeutic agents with a point-of-care diagnostic for blood brain barrier integrity.

In one aspect, the invention provides a peptide comprising a chaperone-mediated autophagy (CMA)-targeting signal domain; a protein-binding domain that selectively binds to a target cytosolic protein; and a cell membrane penetrating domain (CMPD). In another aspect, the invention provides methods for reducing the intracellular expression level of an endogenous target protein in vitro and in an animal, wherein the method involves administration of the peptide. Methods are also provided for treating a pathological condition in an animal, the methods comprising administering the peptide to the animal. In one embodiment, the pathological condition is a neurodegenerative disease. In another embodiment of the invention, the target cytosolic protein is death associated protein kinase 1 and the CMPD is protein transduction domain of the HIV-1 Tat protein.

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.